Antiviral Activity of Medicinal Plant

ANTIVIRAL ACTIVITIES OF MEDICINAL PLANTS B.
Pharma Final Year
VIRAL INFECTIONS
• LIST OF VIRUSES AND VIRAL DISEASES:
A:
Adenovirus
AIDS: Cuteneous lesion associated with AIDS
AIDS related malignant tumours
Alphaviruses causing Encephalitis
Arenavirus
Argentine hemorrhagic fever
Arthropod-borne viral encephalitis
Avian Influenza (Bird Flu)
B:
Bolivian Hemorrhagic Fever
C:
Chickenpox
Chikungunya
Coxsackievirus Infection
Crimean-Congo Hemorrhagic Fever
Cytomegalovirus infection
D:
Dengue
E:
Eastern equine encephalitis
Ebola Virus Infection
Echovirus Infection
Epstein - Barr virus infection
Epstein-Barr Virus Related Malignant Tumors
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ANTIVIRAL ACTIVITIES OF MEDICINAL PLANTS B.Pharma Final Year
F:
Fifth Disease
Filovirus
Flavivirus
G:
German measles
H:
Hand, foot & mouth disease
Hemorrhagic fever with renal syndrome
Herpes Virus(Herpesviridae)
Herpes Simplex Virus Infection
Herpes Zoster Virus (Shingles)
Human Papilloma Virus Associated Epidermal Lesions
Human Papilloma Virus in Cervical Cancer
I:
Infectious Mononucleosis
Influenza
J:
Japanese Encephalitis
K:
Kaposi Sarcoma
Korean Hemorrhagic Fever
Kyasanur Forest Disease
L:
Lassa Fever
Lymphocytic choriomeningitis
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M:
Marburg Virus Disease
Measles
Molluscum Contagiosum
Mumps
Murray Valley encephalitis
N:
Norwalk Virus related Diarrhea
O:
Omsk hemorrhagic fever
Orthomyxoviruses
P:
Parainfluenza Virus Infection
Paramyxovirus
Parvovirus B19 Infection
Picornavirus
Poxviruses
R:
Rabies
Respiratory syncytial virus infection
Rift Valley Fever
Rotavirus diarrhea
Rubella
Rubeola
S:
Smallpox
St. Louis Encephalitis
T:
Tick-borne Encephalitis
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V:
Varicella
Variola
Venezuelan equine encephalitis
Viral hemorrhagic fevers
Viruses in Leukemia and Lymphoma
W:
Western equine encephalitis
West Nile Virus disease
Y:
Yellow Fever
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BRIEF DISCUSSION ABOUT THE INFECTIONS :
Adenovirus
Adenoviruses were first isolated in 1953 by Rowe and co-workers from human adenoids
removed at surgery.
There are 51 immunologically distinct human adenovirus serotypes - (6 species: Human
adenovirus A through F). Many serotypes are not linked to a specific disease.
Human adenoviruses have a capsid with icosahedral symmetry.
Rodlike structures with knobs at the ends protrude from the capsid. The genome of the
virus is a double-stranded DNA linear molecule.When infecting cells in vitro,
adenoviruses are capable of lytic infection, latent infection, and transformation.
Because of the ability to transform cells and to produce tumours in rodents, they have
been considered possible human tumour viruses, but up to now there has been no
evidence that links adenoviruses to human tumours.
AIDS: Cutaneous lesion associated with AIDS

The acquired immune deficiency syndrome (AIDS) is caused by human immune
deficiency virus (HIV) infection, damaging the cell mediated immune system.
Skin is the most commonly affected organ in HIV infection. Cutaneous lesions in HIV
positive patients serve as a marker of HIV infection and also indicates the stage of the
disease.
Opportunistic infection patterns are different in different parts of the world and change
as people migrate.
Opportunistic infections in HIV positive patients have decreased since introduction of the
therapy. Following therapy there is fall in viral titre and increase in CD4 cells. The
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cutaneous conditions improve or decline in incidence after the therapy. In many

developing countries HAART is still not widely available.
Viral:
Molluscum contagiosum: In HIV- positive patients this lesion presents as persistent
umbilicated or verrucous papules, commonly on the head and neck region.
Histopathology reveals cup-shaped lesion containing molluscum bodies. Giant and warty
verrucous mollusca contagiosa are markers of advanced HIV infection.
Herpes Simplex Usually occurs in perianal, genital and orofacial skin. In HIV and HSV
coinfection the lesions last for more than one month. Histopathology reveals numerous
intranuclear and intracytoplasmic nuclear inclusions. Extensive ulceration and
intraepidermal acantholytic vesicles are noted .
Varicela zoster virus infection Clues to HIV and VZV coinfection - The lesions usually
occur in younger patients. These are more severe lesions and of longer duration.
Human papillomavirus infection there is a high incidence of common and anogenital wart
in HIV positive patients. Condylomata acuminata may occur in HIV infected homosexual
men. There is risk of dysplasia in perianal condyloma. Grossly, these lesions may
present as smooth sessile plaques to exophytic cauliflower plaques. Verrucae vulgaris,
multiple plantar warts, flat and filiform warts may be noted in HIV infected patients.
Common warts are frequently present on the bearded area of the face in HIV positive
patients.
Cytomegalovirus: Almost 90% HIV positive patients develop CMV infection.
Histological examination reveals CMV inclusions in endothelial cells and fibroblasts
together with areas of epidermal necrosis .
Oral hairy leukoplakia: Poorly defined projections are noted on the lateral borders of the
tongue.This lesion indicates advanced immunosuppression. Causative organisms include
Epstein-Barr virus, human papillomavirus or candida. Histological examination reveals
some acanthosis and parakeratosis. Large pale staining cells resembling keratinocytes are
present.
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AIDS related malignant tumours

Patients with HIV infection are at increased risk for developing Kaposi's sarcoma, non-
Hodgkin's lymphoma, and several other cancers.
Accumulating data suggest that HIV-infected patients also are at increased risk for
developing Hodgkin's lymphoma, cervical carcinoma in situ (CIS), other anogenital
neoplasms (invasive cancer and CIS), leiomyosarcoma, and conjunctival squamous cell
carcinoma.
AIDS is caused by the human immunodeficiency viruses HIV-I (present globally) and
HIV-II (mainly restricted to West Africa and contacts with that zone).
It is generally assumed that HIV-1 infection play a passive role in cancer development by
impairing the host immune surveillance and increasing the risk of oncogenic virus
infection. Recent insights, however, indicate that HIV-1 infection more actively promotes
cancer growth.
HIV is not per se oncogenic, but a wide range of tumours is now described with increased
incidence among HIV-infected people and/or with a more aggressive clinical course,
compared with HIV-uninfected people.
Kaposi’s Sarcoma (KS):
One of the earliest opportunistic diseases that defined AIDS (even before the etiological
link of AIDS with infection by HIV was recognized) was KS in skin and viscera.
Whether KS is a genuine neoplasm or a reactive hyperplasia of endothelium is still
disputed.
The incidence of KS among HIV-infected people varies with risk-factors for HIV
transmission and geography ; high in homosexual men and African adults and children,
low in haemophiliacs; more frequent in east than West Africa. Epidemiological blood and
tissue studies support its etiological role in development of KS.
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Lymphoma:
High-grade B-cell lymphoma, particularly in the central nervous system, is a major cause
of morbidity and mortality in HIV/AIDS.
Tumours are usually extra-nodal and destructive.
They are commonly associated with Epstein-Barr Virus infection.
Incidence is inversely related to CD4+ T-cell count, which may explain why it is less
common in patients in Africa and India.
T-cell lymphomas, Hodgkin’s disease and myeloma have a slightly increased incidence
compared with HIV-uninfected people.
Conjunctival
Conjunctival carcinoma:
The incidence of conjunctival squamous cell carcinoma is closely related to exposure to

UV light. In equatorial, though not elsewhere, there is an epidemic of this malignancy
among HIV-infected adults. A proven co-factor in a proportion of cases is HPV-16.
Other Tumours:
Small series and case reports of cancers in HIV-infected patients strongly suggest an
increased incidence and more aggressive behavior of other epithelial tumours. These
include skin squamous cell carcinoma and basal cell carcinoma and melanoma. They
are generally present in the later stages of HIV disease. The relative risks for the most
common epithelial cancers in the general population -lung, breast, colon/rectum,
stomach, liver, and prostate - are not increased substantially in people with AIDS,
however.
Most cancers seen in the AIDS setting are related to oncogenic virus infections, such as
Epstein-Barr virus (EBV), Kaposi's sarcoma (KS)-associated herpesvirus (KSHV) and
human papillomavirus (HPV).
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Clinical evidence suggests that the oncogenicity of HPV is altered by the presence of
HIV-1 infection irrespective of host immune status.
Avian Influenza (Bird Flu)

Avian influenza in birds:
It is an infection caused by avian (bird) influenza (flu) viruses. These viruses occur
naturally among wild birds worldwide in their intestines, but they do not get sick. It is
very contagious among birds including domestic birds eg. Chickens, ducks & turkeys and
kill them.
Virus are excreted from infected birds in their saliva, nasal secretions, & feces. Birds
including domestic ones become infected through direct contact with other infected
poultry, or through contact with infected surfaces (such as dirt or cages) or materials
(such as water or feed).
It causes two main forms of diseases in poultry.
Human infection :
“Human influenza virus” is those subtypes that spread widely among humans. There are
only three known a subtypes of influenza viruses (H1N1, H1N2, and H3N2).Viruses are
constantly changing, and they adapt over time to infect and spread among humans.
Avian Influenza A (H5N1):
Subtype Influenza A “H5N1 virus” that occurs mainly in birds, is highly contagious and
are deadly to them. Infections with these viruses have also occurred man.
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Bolivian Hemorrhagic Fever

Bolivian hemorrhagic fever is an acute febrile disease with hemorrhagic manifestations
that are almost identical to those of Argentine hemorrhagic fever . It is a disease endemic
to northeastern Bolivia.
The etiological agent is Machupo virus (MACV, Arenaviridae).
The virus is similar to that which causes Argentine hemorrhagic fever, and its reservoir is
also wild rodents.
Bolivian hemorrhagic fever was first recognized in rural areas of of northern Bolivia
(1959), and there were two major epidemics in Bolivian villages during 1962-64.
Chickenpox
Varicella (chickenpox) is an acute vesicular exanthem caused by the varicella-zoster
virus, an agent that has a worldwide distribution and for which humans are the only
known host. There are no animal reservoirs.
VZV (HHV3) is a neurotrophic alpha-herpesvirus.
VZV is named after : Varicella, an alternative name for chickenpox (the primary VZV
infection) Zoster, another name for shingles (reactivation of latent VZV infection).
Although all age groups are susceptible, in temperate zones chickenpox affects mostly
children and in the tropics mostly young adults. The virus, which is spread through
inhalation of droplets or by direct contact is highly contagious from about 24 hours
before the initial eruption to a week of more thereafter. Although infection with varicella-
zoster virus establishes lifelong immunity and chickenpox does not recur, the latent viral
genome may be activated years later to cause shingles.
No immune persons (usually children) are susceptible to primary infection with varicella-
zoster virus.
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Chickenpox begins as a “silent” infection of the nasopharynx, with local replication of

varicella-zoster virus.
After an incubation period of 10 to 23 days, the virus enters the bloodstream, causing
viremia and a sudden onset of fever, malaise, and anorexia.
In the circulation it seeds reticuloendothelial cells, an effect that leads to secondary waves
of viremia. The virus then disseminates to skin and viscera, and within 24 hours a red
maculopapular eruption develops, usually on the upper trunk and face.
The papules rapidly become clear vesicles with an erythematous base.
In the next 24 hours, the vesicles become cloudy, the eruption begins to itch, and
scratching may rupture the vesicles. Separate crops appear for 3 to 6 days and spread
peripherally. After the last crop, the scabs heal without scarring.
Though vesicles of the skin are generally painless, painful lesions may develop on
mucous membranes, such as the cornea and tympanic membrane.
Complications include pneumonia, encephalitis, hepatitis, carditis, keratitis, orchitis,
arthritis, hemorrhages and acute encephalopathy with fat accumulation in the viscera
(Reye’s syndrome).
Histologically, the skin lesions initially show ballooning of epidermal cells.
Later, unilocular vesicles containing proteinaceous fluid, degenerating cells and syncytial
giant cells are seen.
Cowdry type A intranuclear inclusions are seen in epidermal cells, endothelial cells of
superficial capillaries, reticuloendothelial cells, and fibroblasts.
The affected organs in chicken pox exhibit spherical foci of coagulative necrosis.
At the margin of these necrotic foci, surviving cells contain intranuclear inclusions.
Chikungunya
Chikungunya virus (CHIKV) is a toga virus belonging to the genus alpha virus,
indigenous to tropical Africa and Asia, where it is transmitted to humans by the bite of
infected mosquitoes, usually of the genus Aedes.
Chikungunya (CHIK) fever, the disease caused by CHIKV, was first recognized in
epidemic form in East Africa during 1952-1953.
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Since the beginning of 2006, this crippling mosquito-borne disease (Chikungunya virus
infection) has shown an explosive emergence in nations in the Indian Ocean area. By
March 7, 2006, 157,000 people had been infected in the French island La Reunion, and
the disease had spread to the islands of Seychelles, Mauritius, and Mayotte (French).
Subsequently, the disease appeared in India, China, and European countries.
Infection in Aedes aegypti salivary glands is asymptomatic and lifelong. It is transmitted
by Aedes aegypti to human, there is no human to human transmission.
The disease is highly infectious.
Its main symptoms are sudden onset of chills, fever, headache, rash, and debilitating
arthralgia . The symptoms may persist for several weeks.
The word "chikungunya" is thought to derive from description in local dialect of the
contorted posture of patients afflicted with the severe joint pain associated with this
disease.May rarely cause hemorrhagic fever, specially in children.Incubation period is 1
to 12 days. Fever lasts for 3 - 7 days, arthralgia may persit for upto 3 weeks.
Because CHIK fever epidemics are sustained by human-mosquito-human transmission,
the epidemic cycle is similar to those of dengue and urban yellow fever.
Large outbreaks of CHIK fever have been reported recently on several islands in the
Indian Ocean and in India.
Though fetal contamination risks appear to be rare before 22 weeks of gestation, they are
potentially dangerous. After 22 weeks gestation, newborns infection occurs if the mother
is viremia positive at delivery. Transplacental transmission is suspected, but the
pathogenic mechanism remains unknown.
Warm, humid climates and water reservoirs serve as an excellent breeding ground for the
vector of the virus, Aedes mosquitoes. With an increase in temperature, susceptibility of
mosquitoes to CHIKV increases.
Although the disease is self-limiting, the risk to non-immune travellers from other parts
of the world to areas with a chikungunya epidemic, continues to exist and should be
included in the differential diagnosis of travellers returning home with fever.
Due to similarities in clinical presentation with dengue, limited awareness, and a lack of
laboratory diagnostic capability, CHIKV is probably often under diagnosed or
misdiagnosed as dengue .
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Treatment is supportive. Analgesic and anticonvulsants are often used.The prognosis is

generally good, although some patients experience chronic arthritis. There are very few
recorded fatalities.
With no vaccine or antiviral available, prevention and control depends on surveillance,
early identification of outbreaks, and vector control. CHIKV should be borne in mind in
sporadic cases, and in patients epidemiologically linked to ongoing local or international
outbreaks or endemic areas.
Dengue
Dengue the most prevalent arthropod-borne viral (Arborvirus) disease of humans caused
by four serotypes of dengue virus (DENV 1-4) of the genus Flavivirus.
It is transmitted to man by mosquito Aedes aegypti. It is common in tropical and

subtropical countries, especially in coastal areas. (World distribution of dengue viruses
and their mosquito vector, Aedes aegypti : CDC)
Source: Man is infective to mosquito and mosquito transmits the disease to man.
Echovirus Infection
Echoviruses have been subdivided on the basis of antigenic relationships and differences
in host range into polioviruses , coxsackie viruses groups A and B, and echoviruses.
Echoviruses are RNA viruses of the genus Enterovirus and the family Picornaviridae.
The echoviruses (enterocytopathogenic human orphan viruses) were isolated from faecal
specimens of healthy children.
They produce cytopathic effects in primate cell cultures, but at isolation they were
nonpathogenic for suckling mice or primates.
They are immunologically distinct from polioviruses and have been associated with a
variety of diseases including nonspecific febrile illnesses with or without respiratory
symptoms, aseptic meningitis, paralysis and encephalitis, exanthema, generalized disease
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of new-born and neonatal diarrhea.They also have been associated with chronic meningo-
encephalitis in immaglobulinemic patients.
Flavivirus
The Flaviviridae include almost 70 viruses, nearly half of which have been associated
with human disease. Flavivirus is a genus of the family Flaviviridae.
Flavivirus share a common size (40-60 nanometres), symmetry (enveloped, icosahedra
nucleocapsid), nucleic acid (positive-sense, single stranded RNA approximately 10,000-
11,000 bases), and appearance in the electron microscope.
These viruses are among the most important arthropod-borne viruses worldwide and
include dengue, yellow fever, and Japanese encephalitis viruses.
Morbidity and mortality caused by these viruses vary, but collectively they account for
millions of encephalitis, hemorrhagic fever, arthralgia, rash, and fever cases per year.
Most of the members of this family are transmitted between vertebrate hosts by arthropod
vectors, most commonly mosquitoes or ticks. Transmission cycles can be simple or
complex depending on the hosts, vectors, the virus, and the environmental factors
affecting both hosts and viruses.
German measles
German measles, or rubella, is a mild, systemic infection of childhood.
It is a pleomorphic RNA virus in the Togaviridae family of the genus Rubivirus.
In older children and adults, especially women, it may be more severe, with joint
involvement and purpuric rash. Except for superficial similarity in the name, the rubella
virus is not related to the measles (rubeola) virus.
A worldwide disease, rubella is characterized by measles-like rash, low-grade fever, and
swollen posterior auricular and occipital lymph nodes. The congenital rubella syndrome
(CRS) involves multiple organ systems and has a long period of active infection and virus
shedding in the postnatal period.
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Subclinical infections are common. The incubation period is 12 to 21 days, and the mild
rash and other symptoms resolve within 3 days. Initially, swollen, nontender posterior
auricular and occipital lymph nodes appear. A day or two later the nonpruritic rash begins
on the face and rapidly spreads over the rest of the body, sparing the palms and soles.
The virus is very contagious and is shed from the nasopharynx. The virus is also
transmitted through the placenta, and rubella infections in pregnant women are a serious
public health concern, because intrauterine infection causes spontaneous abortion, fetal
death and a variety of congenital abnormalities. Infection during the first trimester is most
serious. The classic triad of congenital rubella includes ocular abnormalities, heart
disease, and deafness.
The principal congenital abnormalities are patent ductus arteriosus, pulmonary and aortic
stenosis, coarctation of the aorta, defects of the atrial or ventricular septum, ocular lesions
(cataracts, glaucoma, and chorioretinitis), deafness, microcephaly, mental retardation, and
retarded growth. Congenital rubella produces a classic salt-and-pepper pigmentation of
the fundus.
Herpes Simplex Virus Infection

Herpes simplex virus can be divided into two types on the basis of antigenicity,
pathogenicity and genetic properties.
Herpes simplex type II is the major cause of urogenital infections, whereas Herpes
simplex type I is more often isolated from nongenital infections.
Herpes simplex viruses have a worldwide distribution, and direct contact with infected
secretions is the principal mode of spread. Herpes simplex causes disease of the skin and
mucosa such as acute gingivostomatitis, recurrent stomatitis, oral ulcers (cold sores),
herpetic keratoconjunctivitis, herpetic esophagitis, and genital herpes.It also causes
systemic disease as in disseminated herpetic infection of infants, acute necrotizing
encephalitis of the adult, and infections in the immunodeficient host.
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Cytopathologic changes in Herpes infection:

Two types of cytopathology seen in herpes simplex infections are rounding and
degeneration of the cells with inclusion body formation and cell fusion with formation of
syncytia. The intranuclear inclusion is the characteristic cellular lesion, and it consists of
a single, eosinophilic, well-demarcated inclusion body surrounded by a halo and
marginated chromatin.
By electron microscopy the inclusion body consists of paracrystalline arrays of viral
capsids and electron-dense glycoprotein.
Herpetic infection of skin and mucosa:
Herpetic infection of skin and mucosa is manifested by the appearance of red papules that
quickly become vesiculated.
Histologically there is degeneration of the cells in the stratum malpighii and the stratified
squamous epithelium.
In early stages one observes ballooning of the epidermal cells and clearing of the nuclear
chromatin. There is acantholysis and formation of a unilocular vesicle. The typical
inclusion bodies (Cowdry type A) can be seen in the epidermal cells.The upper dermis or
submucosal portions of the affected regions show an inflammatory infiltrate around
capillaries.
The histologic lesion of herpes simplex in skin and mucosa is practically
indistinguishable from that caused by herpes zoster. Immunohistochemistry using
fluorescent antibodies or immuno-peroxidase can, however, make the distinction between
these viruses and even allows typing of the herpesvirus.
Disseminated herpetic disease:

Disseminated herpetic infection of the newborn affects neonates in the first 4 weeks of
life as well as an older group of infants in whom it causes hepatoadrenal necrosis.
Autopsies of infants dying from disseminated herpetic disease show multiple military
foci of necrosis surrounded by hemorrhagic borders in the liver, adrenal gland, and brain.
Microscopically these foci consist of a zone of central coagulative necrosis surrounded by
an area of hyperemia with a sparse mononuclear inflammatory inflammatory reaction.
Inclusion bodies characteristic of the herpetic infection are found in nuclei of the
parenchymal cells surrounding the necrotic zone.
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Pathologic combination may be complicated by the presence of gram-negative

septicemia. Morphologic manifestations of disseminated intravascular coagulation (DIC)
may be also prominent. The virus can be easily easily demonstrated in the lesions by
electron microscopic examination.
Acute necrotizing encephalitis:
Herpes simplex virus has been shown to be a cause of acute necrotizing encephalitis of
the adult. Patients with this syndrome may display a picture of encephalitis or a clinical
picture of an expanding lesion, often of the temporal lobe.
In fatal cases the brain shows asymptomatic necrosis particularly prominent in the
temporal lobes but also involving the hippocampus and the posterior occipital cortex.
Hemorrhage may be prominent. In the early stages of the disease the histopathologic
picture is that of acute necrosis associated with a diffuse meningoencephalitis.
Inclusion bodies within the nuclei of neurons and glial cells can be seen but on occasion
are difficult to find.Reactivation and dissemination of herpetic lesions are not uncommon
in immunocompromised hosts. Esophageal and upper respiratory tract lesions are
commonly found at autopsy in patients who have undergone intense chemotherapy.
Dissemination occasionally occurs, and a picture similar to the disseminated disease in
newborns can be seen.
Dissemination with fatal outcome also occurs in some severely burned patients.
Evidence is accumulating that herpes simplex virus (HSV) infection is implicated in
oncogenesis. HSV antigens have been observed in some oral cancers.
Influenza
Orthomyxoviruses (influenza A, B, and C viruses) are enveloped viruses that contain
single-stranded RNA in a helical array of nucleoprotein. Inserted in the lipid envelop are
two glycoproteins- the hemagglutinin (HA) and the neuraminidase (NA).
Influenza viruses have the unusual capacity of changing the antigenic identities of their
HA and NA polypeptides, thus creating numerous antigenic variants. The host of
different types of virus give their names to the disease, as in, for example, human, swine,
and avian influenza.
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Lassa Fever
The arenavirus Lassa causes a severe illness called Lassa fever. Lassa fever was first
recognized in herdsmen’s village in Nigeria in 1969. Lassa fever is known to be
endemic in Guinea (Conakry), Liberia, Sierra Leone and parts of Nigeria, but probably
exists in other West African countries as well. Lassa fever has been seldom investigated
outside of a few hyperendemic regions, where the described epidemiology may differ
from that in areas of low or moderate incidence of disease.
Lassa fever is a serious, highly infectious, viral, hemorrhagic disease characterized by
high fever, prostration, generalized hemorrhages, abdominal pain, vomiting, diarrhea,
severe pharyngitis, dyspnea, serous effusions, facial edema, and shock. It is fatal in
almost half the cases. Some studies indicate that 300 000 to 500 000 cases of Lassa fever
and 5000 deaths occur yearly across West Africa.
The Lassa virus emerged suddenly and may be a virulent mutant of the lymphocytic
choriomeningitis virus.
Measles
Measles is a highly infectious, systemic infection of childhood, caused by measles virus.
Up to 6 months of age, infants are protected, due to antibodies from mothers, but the
reafter are vulnerable. Measles vaccine has almost eliminated measles.
Mode of infection: Humans are the only natural host.
i) Infection is most commonly transmitted by inhalation of contaminated droplets.
ii) May also be passed through the placenta.
Incubation period: About 14 days (10-21 days).
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Mumps
Mumps is an acute but usually mild viral infection of childhood, characterized by swollen
and inflamed salivary glands (most often the parotids). Less often the virus attacks the
pancreas, ovaries, testes, and other organs. Mump virus is a highly contagious
paramyxovirus that is commonly transmitted in respiratory droplets. A vaccine made
from attenuated live mumps virus has reduced the frequency. Most adults are immune.
Nonimmune adults who acquire the infection may have a painful and debilitating illness.
The incubation period is 2 to 4 weeks, after which fever, headache, malaise, and swelling
and inflammation of the salivary glands follow.Swelling and other acute symptoms
usually subside within 2 weeks. Mumps is usually diagnosed clinically from swollen
salivary glands and confirmed by finding rising titers to mumps virus in the serum of
convalescent patients.
Norwalk Virus related Diarrhea
The prototype “Norwalk agent” was discovered in an outbreak of diarrhea and vomiting
among the elementary school students in Norwalk, Ohio. The virus has icosahedral
symmetry, contains single-stranded RNA, and thought to be a Calicivirus.
Norwalk-like viruses have been associated with gastroenteritis, primarily in adults and
older children. Diarrhea and vomiting are of short duration, and dehydration is rare (as
compared with rotavirus diarrhea ).
The outbreaks have occurred at all times of the year and have been associated with
contaminated water and foods (eg. oysters) infected food-handlers, and person-to-person
spread.
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Poxviruses
The causative viruses are large with a DNA core and a surrounding capsid. Poxvirus
infection occurs in human and animals. These are members of Poxviridae family. There
are two subgroups, based on the morphological features of the virus. The viruses of
molluscum contagiosum and orf are oval or cylindrical in shape and measure
approximately 150x300 nm. The remaining viruses are brick-shaped and range in size in
size from 250 to 300nm x200 to 250 nm.
Clusters of these poxviruses can be identified in hematoxylin and eosin-stained sections
as intracytoplasmic eosinophilic inclusions. The poxviruses fall into different subgroups
depending on antigenic relationships.
Rabies
Rabies viruses are a RNA viruses of the genus Lyssavirus and the family
Rhabdoviradae.
Rabies remains as one of the most feared zoonotic diseases in the world. In humans it is a
lethal encephalitis. Carnivores, such as the dog, wolf, fox, and skunk, are the principal
reservoirs, but the infection extends to bats and to some domesticated animals, such as
cattle, goats, and swine. The infectious agent is transmitted to humans through
contaminated saliva introduced into the wound of a bite.The virus enters a peripheral
nerve and is transported by centripetal axoplasmic flow to the spinal cord and brain.
The latent interval varies in proportion to the distance of transport, being as short as 10
days or as long as 3 months. Centrifugal intra-axonal transport of the virus contaminates
visceral organs, particularly the salivary glands, which in turn contaminate the saliva.
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Rotavirus diarrhea
Rotaviruses contain double-stranded RNA, resemble a wheel, have icosahedral
symmetry, and are “double-shelled” (with inner and outer capsid). Rotavirus particles
have been found in the duodenal mucosa of children with acute gastroenteritis and in
diarrheal stool specimens. In developed countries rotavirus is the most common pathogen
of childhood diarrhea. Rotavirus-induced diarrhea is an endemic problem throughout the
world, the organisms being identified in half the children in developing countries.
In temperate countries rotavirus diarrhea usually has a seasonal winter peak, but in
tropical countries high rates are observed throughout the year.
Nosocomial infections are common, and shedding of rotavirus has been found in some
(usually asymptomatic) newborns in communal obstetric nurseries within 3 to 4 days of
birth.Antibodies to the rotavirus in colostrums and breast milk protect against infection.
The highest incidence of symptomatic infection is in children aged 7 to 24 months. Most
children have rotavirus antibodies by end of the third year, and nearly all infections in
adults are subclinical.
Smallpox
Before its eradication, smallpox (variola) was an acute, highly contagious, exanthematous
viral infection. The virus contains a double-stranded DNA and produces a typical plaque,
or “pock”, when cultured on chorioallantoic membrane of embryonated chicken eggs.
Jenner’s pioneering work in 1796, a similar virus - vaccinia, the causative agent of
cowpox - has been used for “vaccination” to protect against small pox.Smallpox was
evidently an ancient disease; a rash resembling smallpox was found in the mummified
remains of the Egyptian Pharaoh Ramses V, who died in 1160 BC. The disease once had
worldwide distribution in both urban and rural areas, afflicting persons of both genders
and all ages, but particularly children.In 1967, the World Health Organization began its
uniquely successful campaign to eradicate smallpox.
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By then, smallpox had already been controlled in most developed countries but was still
endemic in the less developed world. In 10 years the vaccination campaign eradicated the
disease.
Viral hemorrhagic fevers
Viral hemorrhagic fevers are a group of distinct acute viral infections that cause varying
degrees hemorrhage and shock, and sometimes death. There are many similar viral
hemorrhagic fevers in different parts of the world, often named for the area where they
are first described.
Yellow Fever
Yellow fever (YF) is an infectious, non-contagious disease caused by an RNA virus of
the family Flaviviridae (that cause dengue and other hemorrhagic fevers), which is
transmitted to man by the bite of hematophagous mosquitoes. First described in the
Caribbean, yellow fever is the oldest known viral hemorrhagic fever.It is a re-emerging
infectious disease that currently is at risk of urbanization due to the advance of the Aedes
aegypti vector.
Geographic distribution: The disease affects about 200,000 individuals annually, mainly
in tropical Africa and South America, including both jungle and urban settings.It is a
significant hazard to unvaccinated travelers to these endemic areas. Recent increases in
the density and distribution of the urban mosquito vector, Aedes aegypti, as well as the
rise in air travel increase the risk of introduction and spread of yellow fever to North and
Central America, the Caribbean, the Middle East, Asia, Australia, and Oceania.
Mode of Infection: The usual reservoir is tree dwelling monkeys, virus being passed
among them in the forest canopy by mosqitoes. These monkeys are a good reservoir
because the virus neither kills them nor makes them ill . Humans acquire jungle yellow
fever by entering the forest and being bitten and inoculated by Aedes mosquitoes. Felling
trees increases the risk because mosquitoes are brought down with the tree. On returning
to the village or city, the victim becomes the reservoir for epidemic yellow fever in the
urban setting , where Aedes aegypti is the vector.
22
Hence, virus transmission occurs between humans, mosquitoes, and monkeys. The
mosquito, the true reservoir of YF, is infected throughout its life, and can transmit the
virus transovarially through infected eggs. Man and monkeys, on the other hand, play the
role of temporary amplifiers of the virus available for mosquito infection.
23
List of plants which extract used as antiviral medicine
Species Common name Claim

Acanthopanax Aids digestion, cures hepatitis C, lowers blood
Prickly ginseng, Wujiapi
gracilistylus pressure, increases stamina.
Eaten to counter poisoning, but must be eaten
Achillea millefolium Yarrow
quickly
Agaricus May enhance immune system and have anti-cancer
Agaricus blazei
subrufescens properties (Reviewed by Hetland) ]
Antibiotic (in vitro)/stops infectionNicole Johnston
(April 2002). "Garlic: a natural antibiotic". Modern
Allium sativum Garlic Drug Discovery
Cardiovascular health
Aloe ferox
Anethum graveolens Dill and Dill oil used to soothe the stomach after meals
Amorphophallus Atopic dermatitis

Konjac
konjac high cholesterol
Used for strains, sprains, and bruises. The roots
contain derivatives of thymol,[14] which are used as
Arnica montana Arnica
fungicides and preservatives and may have some
anti-inflammatory effect.
Aquilaria agollocha Eaglewood
Help to prevent the development of parasite
Artemisia annua L. Sweet sagewort resistance,it also has anti-malarial properties, and has
anti-cancer properties
Artemisia
Wormwood Removal of internal parasites
absinthium L.
Aristolochia rotunda Smearwort
Arum maculatum Lords and Ladies
Astragalus
Astragalus
membranaceus
Pain relief, hunger stimulation, wasting caused by
Cannabis, Cannabis sativa,
Cannabis Sativa HIV/AIDS, Glaucoma, nausea, | anticarcinogenic
Marijuana, Hashish
through angiogenesis inhibition through various
24
agents such as tetrahydrocannabinol, cannabidiol,

hexahydrocannabinol, quinone, arachidonyl
ethanolamide
Citrus aurantium
Bergamot orange Malaria
ssp. bergamia
Crataegus spp. L. Hawthorn Nervous tension
Cydonia oblonga Quince
Cymbopogon
Lemon grass
flexuosus
Cymbopogon
Fever grass
schoenanthus
Digitalis lanata Digitalis, Balkan Foxglove Antiarrhythmic agent and inotrope
Purple coneflower, and other Reduce the severity and duration of symptoms
Echinacea purpurea
species of Echinacea associated with cold and flu.
Fevers and inflammations. Pain relief. Ulcers.
Bacteriostatic. Listed as therapeutical in 1652 by
Filipendula ulmaria Nicholas Culpeper. In 1838, salicylic acid was
Meadowsweet
(Spiraea ulmaria) isolated from the plant. The word Aspirin is derived
from spirin, based on Meadowsweet's synonym name
Spiraea ulmaria.
Glycyrrhiza glabra Liquorice
Hydrastis
Goldenseal Antimicrobial
canadensis
Hypericum
St. John's wort Antidepressant
perforatum
Galanga resurrectionlily,
Kaempferia galanga
Shannai
Marrubium vulgare Horehound Expectorant
Matricaria recutita
(Chamomilla Chamomile Relaxant/Calmative
recutita)
Mentha × piperita Peppermint Irritable Bowel Syndrome/Peristalsis
Nepeta cataria Catnip Soothes coughs
Panax Ginseng
Pain relief. Morphine made from the refined and
modified sap is used for pain control in terminal
Papaver somniferum Opium Poppy
patients. Dried sap was used as a traditional medicine
until the 19th century.
25
Passiflora spp. Passion-flower Insomnia

Topical: acne
Phytolacca spp. Pokeweed
Internal: tonsilitis
Plantago spp. Plantain and Psyllium Astringent
Salvia stenophylla Blue Mountain Sage
Poppiocious
Poppy seeds Helps sleeping/relieves pain
seediouphylla
Rosmarinus
Rosemary
officinalis
Ancient medicine, already described by Greek
Salix alba White willow pharmacologist Dioscorides. Bark contains salicylic
acid, which name is derived from Salix.
Symphytum
Comfrey Stops infection
officinale
Improves cognitive function in mild to moderate
Salvia officinalis Sage
Alzheimer's disease.
Tanacetum
parthenium
Feverfew Relieves Migranes, helps fevers and chills.
(Chrysanthemum
parthenium)
Taraxacum
Dandelion Digestive
officinale
Tilia spp. Lime Blossom
Urtica dioica Stinging Nettle
Valeriana officinalis Valerian Sedative
boosts the Immune system, antispasmodic, diuretic,

anodyne, and demulcent Used to treat coughs,
Verbascum thapsus Mullein (protracted) colds, hemoptysis, catarrh, dysentery,
diarrhoea and as a general tonic (like ginseng) to
boost the immune system
Zingiberis rhizoma Ginger can help ease nausea from chemotherapy
26
There are hundreds of plants used all over the world, which are used in herbal medicine
as treatments for viral infections.
Here are some of the most accessible and reliable natural antiviral herbs:
Astragalus (astragalus membranaceus) : has been in the Chinese Materia Medica for
centuries and has shown to have immune boosting properties. This classic energy tonic
has a warming and toning effect. Although not used as a treatment for acute illnesses,
astragalus is believed to be very useful as an herbal remedy for treating viral infections,
including those that cause the common cold and flu.
Echinacea (eucalyptus globulus): has long been used as an antiviral remedy for colds
and flu. It appears to work by boosting production of interferon, the body’s own antiviral
fighter, as well as, stimulating infection-fighting white blood cells. Echinacea has three
compounds, which are chicoric acid, caffeic acid, and echinacin. These three compounds
have specific antiviral properties that can resist viruses.
Forsythia (Forsythia suspensa) and Honeysuckle (Lonicera japonica) are the top choice in
the Chinese Materia Medica for addressing heat toxins. Often used together, these
flowers are the main ingredient in a formula called Yin Qiao San for treating viruses
causing upper respiratory infections.
Garlic (allium sativum): Compounds that are rich in sulfur content are found in
abundance in garlic and are active against the virus responsible for flu. These sulfur-
based compounds have shown to be effective in clinical studies. A similar but less
effective antiviral action is also found in the common onion, which is a close relative of
the garlic plant.
Ginger (zingiber officinale): Phenolic compounds are responsible for relaxing the
muscles of the stomach, and explains ginger‘s effect in easing motion sickness. Fresh or
dried, the root has been shown to minimize vomiting. In addition, the phenolic
ingredients act within the stomach as a sedative and painkiller, which helps to reduce
over-activity of the gut. In stomach infections, the oil acts as an antiseptic and an anti-
27
inflammatory. The gingerols alone are thought to be responsible for ginger‘s action as a
liver protective.
Goldenseal (hydrastis canadensis): Berberine is the active compound in goldenseal that

stimulates the immune system. douche of goldenseal is excellent for reducing yeast
infection. Berberine increases blood flow to the spleen and stimulate the activity of
macrophages, blood cells that are an important part of the immune system.
Licorice (glycyrrhiza glabra): also used for centuries and found in the Chinese Materia
Medica, this herb’s potent antiviral action works against a wide range of viral agents.
With eight active antiviral compounds, the most recognized being glycyrrhizin, these
compounds inhibit as well as block the viral penetration of the body’s cells and the
multiplication of genetic material from the viral particle.
Essential Oils with Antiviral Properties
Use these oils externally by blending a few drops into a base oil of vegetable, sunflower,
safflower or canola oils and massage into pulse points, chest, tops of feet and wrists. Do
not digest these oils internally. Tea tree can be added to a half a cup of warm water and
gargled then spit out for treating sore throats.
Eucalyptus (eucalyptus globulus): this oil has compounds which include quercitrin,
hyperoside, and tannic acid, which help eliminate viruses.
Juniper (juniperus): has an antiviral agent. Juniper contains a potent antiviral compound
called deoxypodophyllotoxi n. The herpes viruse, flu and many other types of viruses
seem to be inhibited by extracts from juniper.
Lemon Balm (melissa officinalis) : is a potent inhibitor on the herpes virus, among other
viruses that lead to infection.
Tea Tree Oil (melaleuca alternifolia) : used for everything from earache to athlete’s
foot, as well as gum inflammation and skin infections, this antiviral oil can be applied
directly to an infected area, three times daily. Tea tree can be added to a half a cup of
warm water and gargled then spit out for treating sore throats.
28
Some important antiviral activity of plants

Antiviral drugs are a class of medication used specifically for treating viral infections.
Like antibiotics, specific antivirals are used for specific viruses. They are relatively
harmless to the host, and therefore can be used to treat infections. They should be
distinguished from viricides, which actively deactivate virus particles outside the body.
Most of the antiviral now available are designed to help deal with HIV; herpes viruses,
best known for causing cold sores and genital herpes, but actually causing a wide range
of diseases; the hepatitis B and C viruses, which can cause liver cancer, and influenza A
and B viruses. Researchers are now working to extend the range of antivirals to other
families of pathogens.
Antiviral drugs work by inhibiting the virus before it enters the cell, stopping it from
reproducing, or, in some cases, preventing it from exiting the cell. However, like
antibiotics, viruses may evolve to resist the antiviral drug.
VIRUS: AN INTRODUCTION
Virus are obligate intracellular organism, contain DNA or RNA within a cylindrical or
spherical protein coat or capsid, which may be surrounded by a lipid bilayer (envelope).
Viruses are organisms that can be characterized as having two distinct phases in their life
cycle - an intracellular and an extracellular phase.
Intracellular phase is the replicative phase during which the virus multiplies in the
infected cell. There it borrows the metabolic machinery of the cell to direct the synthesis
of proteins coded by the viral genome. The structural and nonstructural virion
components are synthesized independently, and the structural proteins are assembled into
whole virions during the final stage of reproduction. When virions leave the cell, they are
particles of uniform size, shape and chemical composition that in some cases can
crystallize. This is the extracellular phase of the virus. The viral particles can initiate the
infectious process of new cells, and hence they constitute the infectious form of the virus.
29
Virus life cycle
Viruses consist of a genome and sometimes a few enzymes stored in a capsule made of
protein (called a capsid), and sometimes covered with a lipid layer (sometimes called an
'envelope'). Viruses cannot reproduce on their own, and instead propagate by subjugating
a host cell to produce copies of themselves, thus producing the next generation.
Researchers working on such "rational drug design" strategies for developing antivirals
have tried to attack viruses at every stage of their life cycles. Some species of mushrooms
have been found to contain multiple antiviral chemicals with similar synergistic effects.[3]
Viral life cycles vary in their precise details depending on the species of virus, but they
all share a general pattern:
• Attachment to a host cell.

• Release of viral genes and possibly enzymes into the host cell.
• Replication of viral components using host-cell machinery.
• Assembly of viral components into complete viral particles.
• Release of viral particles to infect new host cells.
Limitations of vaccines
Vaccines bolster the body's immune system to better attack viruses in the "complete
particle" stage, outside of the organism's cells. They traditionally consist of an attenuated
(weakened or killed) version of the virus. These vaccines can, in rare cases, harm the host
by inadvertently infecting the host with a full-blown viral occupancy. Recently "subunit"
vaccines have been devised that consist strictly of protein targets from the pathogen.
They stimulate the immune system without doing serious harm to the host. In either case,
when the real pathogen attacks the subject, the immune system responds to it quickly and
blocks it.
Vaccines are very effective on stable viruses, but are of limited use in treating a patient
who has already been infected. They are also difficult to successfully deploy against
30
rapidly mutating viruses, such as influenza (the vaccine for which is updated every year)
and HIV. Antiviral drugs are particularly useful in these cases.
Anti-viral targeting
The general idea behind modern antiviral drug design is to identify viral proteins, or parts
of proteins, that can be disabled. These "targets" should generally be as unlike any
proteins or parts of proteins in humans as possible, to reduce the likelihood of side
effects. The targets should also be common across many strains of a virus, or even among
different species of virus in the same family, so a single drug will have broad
effectiveness. For example, a researcher might target a critical enzyme synthesized by the
virus, but not the patient, that is common across strains, and see what can be done to
interfere with its operation.
The target proteins can be manufactured in the lab for testing with candidate treatments
by inserting the gene that synthesizes the target protein into bacteria or other kinds of
cells. The cells are then cultured for mass production of the protein, which can then be
exposed to various treatment candidates and evaluated with "rapid screening"
technologies.
Approaches by life cycle stage
Before cell entry
One anti-viral strategy is to interfere with the ability of a virus to infiltrate a target cell.
The virus must go through a sequence of steps to do this, beginning with binding to a
specific "receptor" molecule on the surface of the host cell and ending with the virus
"uncoating" inside the cell and releasing its contents. Viruses that have a lipid envelope
must also fuse their envelope with the target cell, or with a vesicle that transports them
into the cell, before they can uncoat.
31
This stage of viral replication can be inhibited in two ways:

• Using agents which mimic the virus-associated protein (VAP) and bind to the
cellular receptors. This may include VAP anti-idiotypic antibodies, natural
ligands of the receptor and anti-receptor antibodies.
• Using agents which mimic the cellular receptor and bind to the VAP. This
includes anti-VAP antibodies, receptor anti-idiotypic antibodies, extraneous
receptor and synthetic receptor mimics.
This strategy of designing drugs can be very expensive, and since the process of
generating anti-idiotypic antibodies is partly trial and error, it can be a relatively slow
process until an adequate molecule is produced.
Entry inhibitor
A very early stage of viral infection is viral entry, when the virus attaches to and enters
the host cell. A number of "entry-inhibiting" or "entry-blocking" drugs are being
developed to fight HIV. HIV most heavily targets the immune system's white blood cells
known as "helper T cells", and identifies these target cells through T-cell surface
receptors designated "CD4" and "CCR5". Attempts to interfere with the binding of HIV
with the CD4 receptor have failed to stop HIV from infecting helper T cells, but research
continues on trying to interfere with the binding of HIV to the CCR5 receptor in hopes
that it will be more effective.
Uncoating inhibitor
Inhibitors of uncoating have also been investigated.Amantadine and rimantadine, have
been introduced to combat influenza. These agents act on penetration/uncoating.
Pleconaril works against rhinoviruses, which cause the common cold, by blocking a
pocket on the surface of the virus that controls the uncoating process. This pocket is
similar in most strains of rhinoviruses and enteroviruses, which can cause diarrhea,
meningitis, conjunctivitis, and encephalitis.
During viral synthesis
A second approach is to target the processes that synthesize virus components after a
virus invades a cell.
32
Reverse transcription
One way of doing this is to develop nucleotide or nucleoside analogues that look like the
building blocks of RNA or DNA, but deactivate the enzymes that synthesize the RNA or
DNA once the analogue is incorporated. This approach is more commonly associated
with the inhibition of reverse transcriptase (RNA to DNA) than with "normal"
transcriptase (DNA to RNA).The first successful antiviral, acyclovir, is a nucleoside
analogue, and is effective against herpesvirus infections. The first antiviral drug to be
approved for treating HIV, zidovudine (AZT), is also a nucleoside analogue.
An improved knowledge of the action of reverse transcriptase has led to better nucleoside
analogues to treat HIV infections. One of these drugs, lamivudine, has been approved to
treat hepatitis B, which uses reverse transcriptase as part of its replication process.
Researchers have gone further and developed inhibitors that do not look like nucleosides,
but can still block reverse transcriptase.Another target being considered for HIV
antivirals include RNase H - which is a component of reverse transcriptase that splits the
synthesized DNA from the original viral RNA .
Integrase
Another target is integrase, which splices the synthesized DNA into the host cell genome.
Transcription
Once a virus genome becomes operational in a host cell, it then generates messenger
RNA (mRNA) molecules that direct the synthesis of viral proteins. Production of mRNA
is initiated by proteins known as transcription factors. Several antivirals are now being
designed to block attachment of transcription factors to viral DNA.
Translation / antisense
Genomics has not only helped find targets for many antivirals, it has provided the basis
for an entirely new type of drug, based on "antisense" molecules. These are segments of
DNA or RNA that are designed as complementary molecule to critical sections of viral
genomes, and the binding of these antisense segments to these target sections blocks the
operation of those genomes. A phosphorothioate antisense drug named fomivirsen has
33
been introduced, used to treat opportunistic eye infections in AIDS patients caused by
cytomegalovirus, and other antisense antivirals are in development. An antisense
structural type that has proven especially valuable in research is morpholino antisense.
Morpholino oligos have been used to experimentally suppress many viral types:
• caliciviruses
• flaviviruses (including WNV)
• dengue
• HCV
• coronaviruses
Translation / ribozymes
Yet another antiviral technique inspired by genomics is a set of drugs based on

ribozymes, which are enzymes that will cut apart viral RNA or DNA at selected sites. In
their natural course, ribozymes are used as part of the viral manufacturing sequence, but
these synthetic ribozymes are designed to cut RNA and DNA at sites that will disable
them.
A ribozyme antiviral to deal with hepatitis C has been suggested, and ribozyme antivirals
are being developed to deal with HIV.[13] An interesting variation of this idea is the use of
genetically modified cells that can produce custom-tailored ribozymes. This is part of a
broader effort to create genetically modified cells that can be injected into a host to attack
pathogens by generating specialized proteins that block viral replication at various phases
of the viral life cycle.
Protease inhibitors
Some viruses include an enzyme known as a protease that cuts viral protein chains apart
so they can be assembled into their final configuration. HIV includes a protease, and so
considerable research has been performed to find "protease inhibitors" to attack HIV at
that phase of its life cycle.[14] Protease inhibitors became available in the 1990s and have
34
proven effective, though they can have unusual side effects, for example causing fat to
build up in unusual places. Improved protease inhibitors are now in development.
Protease inhibitors have also been seen in nature. A protease inhibitor was isolated from
the Shiitake mushroom (Lentinus edodes).The presence of this may explain the Shiitake
mushrooms noted antiviral activity in vitro.
Assembly
Rifampicin acts at the assembly phase.
Release phase
The final stage in the life cycle of a virus is the release of completed viruses from the host
cell, and this step has also been targeted by antiviral drug developers. Two drugs named
zanamivir (Relenza) and oseltamivir (Tamiflu) that have been recently introduced to treat
influenza prevent the release of viral particles by blocking a molecule named
neuraminidase that is found on the surface of flu viruses, and also seems to be constant
across a wide range of flu strains.
Immune system stimulation
A second category of tactics for fighting viruses involves encouraging the body's immune
system to attack them, rather than attacking them directly. Some antivirals of this sort do
not focus on a specific pathogen, instead stimulating the immune system to attack a range
of pathogens.One of the best-known of this class of drugs are interferons, which inhibit
viral synthesis in infected cells.[19] One form of human interferon named "interferon
alpha" is well-established as part of the standard treatment for hepatitis B and C,[20] and
other interferons are also being investigated as treatments for various diseases.
A more specific approach is to synthesize antibodies, protein molecules that can bind to a
pathogen and mark it for attack by other elements of the immune system. Once
researchers identify a particular target on the pathogen, they can synthesize quantities of
identical "monoclonal" antibodies to link up that target. A monoclonal drug is now being
35
sold to help fight respiratory syncytial virus in babie and antibodies purified from
infected individuals are also used as a treatment for hepatitis B.
Aids
The acquired immune deficiency syndromes (AIDS) is the state of profound immuno-
suppression produced by chronic infection with the human immune deficiency virus
(HIV). It is characterized by profound immunosuppression that leads to opportunistic
infections, secondary neoplasm and neurologic manifestations.
Plants Used in Treating HIV
While new drugs are constantly being produced and studied for the treatment of HIV, or
human immunodeficiency virus, the use of plants is not out of the question. Plants are
still being used in developing nations in the hopes of treating, and one day curing, HIV.
Herbs
1. Herbal medicinal remedies have been used for centuries to treat a variety of ailments in
various cultures. Aloe vera, St. John's Wort, echinacea and ginseng have been used to
boost the immune system. Ginkgo, garlic and astragalus also help revive a failing
immune system.
Licorice
2. Licorice, or deglycyrrhizinated licorice, has a soothing effect on the mouth and throat for
HIV and AIDS patients suffering from ulcers in these places.
Astragalus Root
3. A Chinese herb, the astragalus root has been used in the East to prevent and slow the
shortening of telomere in immune cell chromosomes. Since HIV attacks the body's
immune cells, the use of the root is now being turned toward this virus. Experts believe
36
the root can be added successfully to anti-retroviral therapies for HIV-positive persons or
perhaps replace them entirely for a lower cost.
Cat's Claw
4. A woody Peruvian vine used by the Ashanica Indians has been proven to reduce the side
effects of AZT therapy for HIV and AIDS patients. Known as cat's claw, it stimulates the
immune system's response to the disease.
South African Plant
5. Known as Sutherlandia frutescens, the South Africa native plant is being used as
an immune and energy booster for sufferers of HIV and AIDS. It is also an
effective anti-depressant.
Materials and methods

Plant material
Seventeen plants (Table 3.2) which are used to treat, HIV- infections in
immunocompromised patients were collected from different areas in Mozambique
Preparation of plant extracts
Dried powdered plant materials wer e extracted with acetone .Fifty grams of powdered
plant material was extracted with 500 ml of solvent over two days under reflux.
The extracts were then filtered and concentrated to dryness under reduced pressure
and the residues freshly dissolved in an ap propriate solvent on the day that the bioassay
was done.
HIV-1 Reverse tra nscriptase (RT) assay
The effect of plant extracts on RT activity in vitro was evaluated with a non-
radioactive HIV-RT colorimetric ELISA kit (Roche, Germany). The assay was carried out
in triplicate. Adriamycin, an anticancer drug and also an inhibitor of viral reverse
37
transcriptase (Goud etal ., 2003) was used as a positive control.In each test well,
2µl of diluted recombinant HIV-1 reverse transcriptase (4-6 n g), 20µl o f diluted
extract, and 20µl o freaction mixture was dispensed. The final concentration of each
extract in each well was 20 µg/ml. Since this part of the experiment was not
conducted at the University of Pretoria, but at Nelson Mandela Metropolitan
University; due to cost implications, only one concentration was selected. Negative
control wells contained 40µl of lysis buff er and 20µl of reaction mixture. The
concentration of positive drug control (Adriamycin) was 100µ g/ml. Positive control
wells contained 20µl diluted recombinant HIV-1 Reverse transcriptase (4-6 ng), 20µl of
lysis buffer containing 10% DMSO, and 20µl o f reaction mixture. The wells of the
micro titer plate modules were washed five times with 250µl of washing buffer per well
for 30 seconds each. The washing buffer was then carefully removed and 200 µ l of anti-
DIG-POD working solution was dispensed into each well. Incubation at 37oC followed
once again for 1 hour after the micro titer plate modules were covered with foil. The
wells were then washed in the same manner as before, the washing buffer was
carefully removed from the wells, and 200µl of ABTS substrate was dispensed into
the wells. Incubation then commenced for 10-30 min at room temperature (15-25 C). The
absorbencies of the samples were measured at 405nm( reference wavelength: 492
nm). The percentage inhibitory activity of the extracts samples were then calculated,
with reference to the positive control.
Herpes simplex
Plant Extracts Antiviral Activity against Herpes simplex
PLANT EXTRACTS ANTIVIRAL ACTIVITY AGAINST HERPES SIMPLEX VIRUS

TYPE 1 AND AFRICAN SWINE FEVER VIRUS
ABSTRACT
38
Twenty-eight extracts prepared from plants used in African traditional medicine and from
Rhamnus glandulosa Ait. of the Portuguese flora, were screened in order to assay their
antiviral activity against Herpes simplex virus type 1 (HSV-1) and African swine fever
virus (ASFV). Twelve of these extracts revealed virucidal activity against HSV-1
whereas only six have the same activity against ASFV. Further studies showed that
thirteen of the tested extracts inhibited HSV-1 infection, some of which had a significant
activity against this virus such as Senna podocarpa (Guill. & Pert.) Lock, Cassia
sieberiana DC., Guiera senegalensis J.F. Gmel., Piliostigma thonningii (Schum.) Milne-
Redhead, Rhamnus glandulosa Ait. and Uvaria chamae P. Beauv. Four of the twenty-one
tested extracts inhibited ASFV infection
MATERIALS AND METHODS
Plant Materials
Plants were collected in Guinea-Bissau and identified by Dr. A. Diniz; voucher

herbarium specimens have been preserved in LISC Herbarium of the "Centro de Botânica
Tropical", Lisbon, Portugal; Rhamnus glandulosa leaves were collected by Mr. N¢brega
from a plant specimen of "Jardim Botânico do Funchal", Madeira Island, Portugal.
Extracts Preparation
Different parts of the dried plants were extracted with ethanol at room temperature and
concentrated under reduced pressure (temperature < 40øC). The dried extracts were
dissolved in dimethylsulfoxide (DMSO) at a concentration of 100 mg/ml.
Cells Used
Vero cells were obtained from the American Type Culture Collection and were grown as
monolayers in Dulbecco's Modified Eagle Medium (DME) (Gibco, Scotland)
supplemented with 10% of New-born Calf Serum (NCS) (Gibco, Scotland) and
gentamicin (50 æg/ml).
Viruses
39
African swine fever virus (ASFV), strain Lisbon 60, was originally obtained in 1960
from an infected pig in Lisbon (Ribeiro and Azevedo, 1961), adapted to grow in monkey
cells and was cloned by four successive plaque purification in Vero cells, as described by
Enjuanes et al. (1976). Herpes simplex virus type 1 (HSV-1, clinical strain) stocks were
prepared in Vero cells in DME supplemented with 2% NCS. Only the extracellular
viruses were used, after low speed centrifugation of cell debris. When necessary, vires
suspensions were concentrated by centrifugation at 11000 G for 6 h at 4øC. Plaque
titrations were done as described by Enjuanes et al. (1976).
Antiviral Assays
Cytotoxicity assays -- As a first step, the cytotoxicity of the extracts was evaluated in
order to determine their maximum tolerated concentration (MTC) to Vero cells. Vero
Cell monolayers in 96-well plates (Nunc, England) were incubated with decreasing
concentrations of the extracts (dissolved in DMSO) for 48 h at 37øC. After 48 h, a dye
uptake assay (Finter, 1969) was performed to determine the percentage of living cells in
relation to the control (cells incubated with DMSO).
Virucidal activity of plant extracts -- The direct effect of plant extracts on HSV-1 and
ASFV was determined by incubating both viruses for 1 h at 37øC with the extracts at the
MTC. The extracts were removed by centrifugation (53,000 G or 100,000 G) and
virucidal activity was determined by plaque titration. Controls were performed by
incubating the viruses with Phosphate Buffered Saline-A (PBS-A) solution (Dulbecco
and Vogt, 1954).
Effect of plant extracts on viral replication -- Vero cell monolayers were incubated for 30
min at 37øC with the extracts at MTC. The extracts were removed and the cells washed
with PBS-A or DME2 (DME supplemented with 2% NCS) at the same temperature. Cell
monolayers were infected with HSV-1 or ASFV at a multiplicity of infection (m.o.i.) of 1
in the presence of the extracts. After adsorption of the viruses for 2 h at 37øC, the
remaining viruses were removed and cells were again washed with PBS-A. The plates
were incubated at 37øC until an extensive cytopathic effect was observed in control
40
(without extract) wells. The media from all infected wells were recovered and titrated for
virus.
Effect of plant extracts on viral adsorption -- Vero cell monolayers were pre-cooled at
4øC for 15 min after which they were infected with HSV-1 in presence of the extracts.
After viral adsorption for 2 h at 4øC, the remaining virus was removed and cells washed
with PBS-A. They were then incubated for a further 24 h at 37øC with DME2 and later
the progeny virus was plaque titrated.
All the experiments were effectuated in duplicate.
Chikungunya Treatment in Plants

Ayurveda is the traditional indian medicine and is a popular alternative medicine in India.
Ayurveda medicines are usually vegetable drugs and hence side effects usually are
minimal. But patients have to be very careful since there are a large number of unlicensed
ayurveda practitioners and some of them are known to add steroids in medicines for
quick benefit.
In Ayurveda Chikungunya is known as Sandhijwara which literally means "fever of the

joints". The symptoms of Sandhijwara and Chikungunya are very similar and hence
Ayurveda treatment provides relief for the disease. The medicines usually prescribed for
fighting the fever are Vilvadi Gulika, Sudarsanam Gulika and Amritarishta. Some
practitioners claims that Chikungunya can be cured faster with Ayurveda treatment. Since
there is no treatment in modern medicine, people consult Ayurveda practitioners for fever
relief in many parts of India. In ayurveda, Chikungunya is considered as a ' vata doksha'
disorder. Diet changes usually prescribed include increased intake of fluid food,
increased intake of vegetables, reduced use of oil and avoiding intake of tea and coffee.
Some practitioners of Ayurveda claim that a medicine called Panchathikta Kashayam can
cure Chikungunya. It is a very bitter drug. Ayurveda massage is also administered for
joint pain relief.
41
Herbs such as Sacred Basil (Tulsi), Carrot and Grapes are usually recommended as a
relief for the pain and fever. Since these are natural herbs there is little risk in trying them
out.
Natural plants
plants for Chicken Pox
Chicken pox is a highly contagious disease affecting mostly children and sometimes
adults also. The rash appears on the body 2 days after the person gets infected. It mainly
occurs during winter and spring season. The duration of this disease ranges from ten to
twenty-one days but is usually between fourteen and seventeen days.
Symptoms of Chicken Pox
Following are the major chicken pox symptoms:
1. Low grade fever

2. Mild headache and weakness
3. Rash appears on the upper chest or back
Causes of Chicken Pox

Following are the major chicken pox causes:
1. Virus infection
2. Wrong feeding of children
Chicken Pox Treatment and Advice
1. Take Raw fruit, vegetable juices and lemon juice
2. Keep the patient in a well-ventilated room
3. Lukewarm water baths can be given every day to relieve itching. For better results,
neem leaves can be added to this water.
42
Herbal Remedies for Chicken Pox
1. Prepare herbal tea by any of the herbs like chamomile (babunah), basil (tulsi),
marigold (zergul) and lemon balm (billilotan). A little cinnamon (dalchini), honey, and
lemon may be added to this tea. It should be sipped slowly several times a day. It is an
effective herbal remedy for chicken pox.
43
Antiviral activity
Of
Medicinal plants
Of
Nilgiris
44
There is an increasing need for search of new compounds with antiviral activityas the treatment
of viral infections with the available antiviral drugs is often unsatisfactory due to the problem of
viral resistance2 coupled with the problem of viral latency and conflicting efficacy in recurrent
infection in immunocompromised patients. Ethnopharmacology provides an alternative approach
for the discovery of antiviral agents, namely the study of medicinal plantswith a history of
traditional use as a potential source of substances with significant pharmacological and biological
activities4. The Indian subcontinent is endowed with rich and diverse local health tradition, which
is equally matched with rich and diverse plant genetic source5. A detailed investigation and
documentation of plants used in local health traditions and ethnopharmacological evaluation to
verify their efficacy and safety can lead to the development of invaluable herbal drugs or isolation
of compounds of therapeutic value. A number of compounds extracted from various species of
higher plants have shown antiviral activity; Examples included tannins7, flavones8, alkaloids, that
displayed in vitro activity against numerous viruses. It has been suggested that selection of plant
on the basis of ethnomedical considerations gives a higher hit rate than screening programmes of
general synthetic products10. Bacopa monneri has been used in conditions like epilepsy, insanity,
nervous disorders11, Hypercicum hookerianum in anxiety and inflammation11, Usnea complanta
and Tagetes minuta for bacterial infections, Santolina chamaecyparissus as a stimulant,
vermifuge and a stomachic.A number of plant extracts reported in traditional medicine to have
antiinfective properties were studied in our laboratory15-19 and were also screened for antiviral
activity. Herpes simplex viruses (HSV) are ubiquitous agents which cause a variety of diseases
ranging in severity from mild to severe, and in certain cases, these may even become life
threatenings, especially in immunocompromised patients. After primary infection, HSV persists
in the host for the lifetime. HSV infection is thus considered lifelong infection. Nucleoside
analogues such as aciclovir (ACV), penciclovir etc., are the only approved drugs for the treatment
of HSV infections. However, the widespread use of nucleoside based drugs has led to the
emergence of resistance in HSV especially among immunocompromised patients. In a recent
survey from Taiwan, the incidence of ACVresistant HSV strains was found to be around 5 per
cent among immunocompromised patients and 14 per cent among bone marrow transplant
recipients. This indicates the need for search of newer antiviral agents to treat such infections.
The present study was undertaken to test the extracts of 18 plants for their antiviral activity
against herpes simplex virus type I (HSV-1, a DNA virus).
45
Material & Methods

Plant materials, reagents, cell line and virus: The plant materials were collected from in and
around Ootacamund, Tamil Nadu, India and were authenticated by the Botanical Survey of India,
Government Arts College, Ootacamund where sample specimens were deposited. Extracts of
different plants were prepared by using Soxhlet extraction unit (Borosil, Mumbai) as per the
standard procedure21. The essential oils from different parts of plants were isolated by water
distillation using Clavenges apparatus (Borosil, Mumbai)22. Eagle's minimum essential medium
(EMEM), trypsin, penicillin, streptomycin and amphotericin B were purchased from Hi-media
Labs, Mumbai, India. 3-(4, 5- dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) and
trypan blue dye were purchased from Sigma, USA. New born calf serum (NBCS) was procured
from PAA Labs, Austria. Vero cells (African green monkey kidney cell) were obtained from
Pasteur Institute of India, Coonoor. Vero cells were grown in EMEM supplemented with Earle's
salts and 10 per cent heat inactivated NBCS, 100 IU/ml penicillin, 100µg/ml streptomycin and
5µg/ml amphotericin B. The cells were maintained at 37ºC in a humidified atmosphere with 5 per
cent CO2 and were subcultured twice a week. HSV-1 was from the collection of the Christian
Medical College and Hospital, Vellore. The virus was propagated in Vero cells and the infective
titre of the stock solution was 10-7 TCID50/ml (50% tissue culture infective dose).
Cytotoxicity assay: Each extract was separately dissolved in 1 ml of distilled dimethyl sulphoxide
(DMSO) and volume was made up to 10 ml with maintenance medium to obtain a stock solution
of 1 mg/ml concentration, sterilized by filtration and further dilutions were made from the stock.
The cytotoxicity assays were carried out using 0.1ml of cell suspension, containing 10,000 cells
seeded in each well of a 96-well microtitre plate (Tarsons India Pvt. Ltd., Kolkata). Fresh
medium containing different concentrations of the test sample was added after 24 h of seeding.
Control cells were incubated without test sample and with DMSO. The little percentage of
DMSO present in the wells (maximal 0.2%)
was found not to affect the experiment. The microtitre plates were incubated at 37ºC in a
humidified incubator with 5 per cent CO2 for a period of 72 h. Sixteen wells were used for each
concentration of the test sample. The morphology of the cells was inspected daily and observed
for microscopically detectable alterations, i.e., loss of monolayer, granulation and vacuolization
in the cytoplasm. The cytopathogenic effect (CPE) was scored. The 50 per cent cytotoxic
concentration (CTC50), was determined by the standard MTT assay23,24, trypan blue dye exclusion
method25, cell metabolic function by protein estimation26, and total cellular DNA content by H
thymidine labeling.
46
Antiviral assay: Different nontoxic concentrations of test drugs, i.e., lower than CTC50 were
checked for antiviral property by cytopathic effect (CPE) inhibition assay28 and virus yield
reduction assay29 against different virus challenge doses of 2, 10 and 100 TCID50. In CPE
inhibition assay, cells were seeded in a 96-well microtitre plate with 10,000 cells per well,
incubated at 37ºC in a humidified incubator with 5 per cent CO2 for a period of 48 h. The plates
were washed with fresh MEM and challenged with different virus challenge doses and incubated
at 37ºC for 90 min for adsorption of the virus. The cultures were treated with different dilutions
of plant extracts in fresh maintenance medium and incubated at 37ºC for five days. Every 24 h the
observation was made and cytopathic effects were recorded. Anti-HSV-1 activity was determined
by the inhibition of cytopathic effect compared with control, i.e., the protection offered by the test
samples to the cells was scored. In virus yield assay, reduction in the yield of virus when cells
were treated with the plant extracts was determined.
47
Antiviral Activity
of
Brazilian Plant
48
Unlike antimicrobial drugs against bacteria and fungi, only a few effective antiviral drugs
are available. One of the most important reasons for the lack of success in developing
antiviral drugs is due to the nature of the infectious viral agents, which totally depend
upon the cell they infect for their multiplication and survival, so that many compounds
that may cause the death of viruses also are very likely to injure the host cell that harbour
them .
On of the possible method which can be used for the discovery of active substances is the
screening of plant extracts for antiviral activity followed by bioassay guided fractionation
of active extracts to identify the active substance.
In searching for natural products as potential antiviral agents, several medicinal plants
from the South American folk medicine showed in vitro antiviral activity 2-4. In an effort
to discover new compounds, with relevant anti-herpes virus activity, the aim of our study
was to examine the potential antiviral activity of native species from South Brazil. The
species were selected mainly on the,basis of their ethnopharmacological indications for
treatment of viral infections such as influenza virus, bronchopulmonary infections and
cold, but some others species were collected randomly. In this study, hydroethanolic and
aqueous crude extracts from fifty species were screened for in vitro antiviral activity
against herpes simplex virus type I (HSV-1) in Vero cell line.
MATERIALS AND METHODS

Plant material
The plants tested were collected from the Rio Grande do Sul State area, Brazil.
Herbarium specimens are deposited in the Herbarium of the Federal University of Rio
Grande do Sul, Brazil (ICN). The air-dried plant materials were
grounded and extracted by maceration in 50% ethanol. An aqueous extract was also
prepared with dried plant material (100 g) in hot distilled water not exceeding 60 °C (200
ml). The extracts were filtered, the ethanol removed, lyophilized and stored at –20 °C
until tested.
Cells and viruses
African green monkey kidney cells (Vero cellline ATCC CCL-81) were grown in Eagle’s
minimum essential medium (MEM) supplemented with 10 % newborn calf serum, 2 µg.
ml–1 of amphotericin B and 10 mg.ml–1 of enrofloxacin. A virus stock of herpes simplex
49
virus type I, strain KOS (University of Rennes/France), ATCC-VR733 and 29R-acyclovir

resistant were prepared on Vero cells infected at a low multiplicity of infection, incubated
for 1 to 2 days, frozen/thawed three times, before clearing the preparation by
centrifugation at low speed to remove the cell debris. Virus stocks were maintained in
liquid nitrogen until use. Virus titration was performed by Kärber method 5 using a 96-
well microtitre plates. The virus titre was estimated from cytopathogenicity and
expressed as
50% tissue culture infectious doses (TCID50.ml–1). It was 10–6 TCID50.ml–1 for strain
KOS; 10–4 TCID50.ml–1 for strain ATCC and 10–4 TCID50.ml–1 for strain 29R-
acyclovir resistant.
Evaluation of cytotoxicity
To assess the effect of extracts on uninfected Vero cells, dilutions ranging from 40
mg.ml–1 to 0.15 µg.ml–1 in the MEM medium, were added to Vero monolayer’s (using a
96-well micro plate with 4.0 x 104 cells per well). After 72 h of incubation at 37 °C,
cytotoxicity was determined by microscopic examination of cell morphology in treated
and untreated cultures. The concentration of the extract at which the cell number was
reduced to 50% of the controls, was taken as the 50% cytotoxic concentration (CC50).
The maximum concentration at which no reduction on cell numbers was observed
(compared to controls) was considered as the maximum tolerated concentration (MTC) 6-
9. The MTC was determined for each extract before proceeding to make antiviral activity
assays. All assays were
carried out in quadruplicate.
Antiviral activity
Dilutions of the extracts were prepared starting from the previously determined MTC.
Extracts from MTC, MTC/2, MTC/4, MTC/8 and MTC/16 were added on confluent 24 h
old monolayers of Vero cells grown in microtitre tissue
culture plates just before virus inoculation. One hundred tissue culture infection doses per
50 ml (TCID50) of the HSV-1 KOS strain were added to each of the wells. Toxicity
controls, cell and virus controls titration were rum simultaneously. All assays were
carried out in quadruplicate. When some antiviral activity was detected
on HSV-1 strain KOS, the extracts were also tested against strain ATCC-VR733 and 29
Racyclovir resistant. Plates were incubated for 72 h at 37 °C, and then examined for the
50
presence of cytopathic effects (CPE). The concentration of extract which inhibited 100%
of the viral CPE (compared to the controls) was considered as the active concentration.
Discussion
51
Conclusion
52
Reference
6. Vanden Berghe DA, Vlietinck AJ, Vanhoof L. Plant products as potential antiviral
agents. Bull Inst Pasteur 1986; 84 : 101-47.
7. De Clercq E. Antiviral agents: characteristic activity spectrumdepending on the
molecular target with which they interact.Adv Virus Res 1993; 42 : 1-55.
8. Field AK, Biron KK. The end of innocerice revisited: resistance of herpesvirus to
antiviral drugs. Clin Microbiol Rev 1994;7 : 1-13.
9. Vlietinck AJ, Vanden Berghe DA. Can ethnopharmacology contribute to the
development of antiviral drugs? J Ethnopharmacol 1991; 32 : 141-53.
10. Pushpangadan P. Role of traditional medicine in primary health care. In: Iyengar PK,
Damodaran VK, Pushpangandan P, editors. Science for health. Trivandrum: State
Committee on Science, Technology and Environment, Government of Kerala; 1995.
11. Hudson JB. Antiviral compounds from plants. Boca Raton, Florida: CRC Press; 1990 p.
200.
12. Fukuchi K, Sakagarmi H, Okuda T, Hatano T, Tanuma S, Kitajima K, et al. Inhibition of
herpes simplex virus infection by tannis and related compounds. Antiviral Res 1989; 11 :
285-97.
13. De Rodriguez DJ, Chula J, Simons C, Armoros M, Veriohe AM, Girre L. Search for in
vitro antiviral activity of a newisoflavone glycoside from Vlex europeus. Planta Med
1990;50 : 59-62.
14. Spedding G, Ratty A, Middleton E Jr. Inhibition of reverse transcriptases by flavonoids.
Antiviral Res 1989; 12 : 99-110.
15. Vanden Berghe DA, Vlietinek AJ. Screening methods for antibacterial an antiviral agents
from higher plants. In: Hostettmann K, editor. Methods in biochemistry. vol 6. London:
Academic Press; 1991 p. 47.
16. Boucher CA, Cammack N, Schipper P, et al. High-level resistance to (-) enantiomeric 2'-
deoxy-3'-thiacytidine in vitro is due to one amino acid substitution in the catalytic site of
HIV type 1 reverse transcriptase. Antimicrobial Agents Chemother 1993, 37:2231-2234.
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17. Brinkman K, Smeitink JA, Romijn JA, Reiss P. Mitochondrial toxicity induced by
nucleoside-analogue reverse-transcriptase inhibitors is a key factor in the pathogenesis of
ART-related lipodystrophy. Lancet 1999, 354:1112-5.
18. CAESAR Co-ordinating Committee. Randomised trial of addition of lamivudine or
lamivudine plus loviride to zidovudine-containing regimens for patients with HIV-1
infection: the CAESAR trial. Lancet 1997, 349:1413-1421. Carr A, Chuah J, Hudson J, et
al. A randomised, open-label comparison of three HAART regimens including two
nucleoside analogues and indinavir for previously untreated HIV-1 infection: the
OzCombo1 study. AIDS 2000, 14: 1171-80.
19. Carr A, Martin A, Ringland C et al. Long-term changes in lipodystrophy after switching
from thymidine analogues to abacavir. Antiviral Therapy 8:L15, 2003.
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patients with HIV lipoatrophy: a randomized trial. JAMA 2002, 288:207-15.
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54

Antiviral Activity of Medicinal Plant

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ANTIVIRAL ACTIVITIES OF MEDICINAL PLANTS B.

Pharma Final Year

BRIEF DISCUSSION ABOUT THE INFECTIONS :

AIDS: Cutaneous lesion associated with AIDS

cutaneous conditions improve or decline in incidence after the therapy. In many

AIDS related malignant tumours

Kaposi’s Sarcoma (KS):

The incidence of conjunctival squamous cell carcinoma is closely related to exposure to

Avian Influenza (Bird Flu)

It causes two main forms of diseases in poultry.

Avian Influenza A (H5N1):

Bolivian Hemorrhagic Fever

The etiological agent is Machupo virus (MACV, Arenaviridae).

Chickenpox begins as a “silent” infection of the nasopharynx, with local replication of

Treatment is supportive. Analgesic and anticonvulsants are often used.The prognosis is

It is transmitted to man by mosquito Aedes aegypti. It is common in tropical and

Herpes Simplex Virus Infection

Cytopathologic changes in Herpes infection:

Disseminated herpetic disease:

Pathologic combination may be complicated by the presence of gram-negative

Norwalk Virus related Diarrhea

Viral hemorrhagic fevers

List of plants which extract used as antiviral medicine

Species Common name Claim

Amorphophallus Atopic dermatitis

agents such as tetrahydrocannabinol, cannabidiol,

Passiflora spp. Passion-flower Insomnia

boosts the Immune system, antispasmodic, diuretic,

Zingiberis rhizoma Ginger can help ease nausea from chemotherapy

Goldenseal (hydrastis canadensis): Berberine is the active compound in goldenseal that

Essential Oils with Antiviral Properties

Some important antiviral activity of plants

Virus life cycle

• Attachment to a host cell.

Approaches by life cycle stage

Before cell entry

This stage of viral replication can be inhibited in two ways:

Yet another antiviral technique inspired by genomics is a set of drugs based on

Rifampicin acts at the assembly phase.

Immune system stimulation

Plants Used in Treating HIV

South African Plant

Materials and methods

HIV-1 Reverse tra nscriptase (RT) assay

Plant Extracts Antiviral Activity against Herpes simplex

PLANT EXTRACTS ANTIVIRAL ACTIVITY AGAINST HERPES SIMPLEX VIRUS

MATERIALS AND METHODS

Plants were collected in Guinea-Bissau and identified by Dr. A. Diniz; voucher

All the experiments were effectuated in duplicate.

Chikungunya Treatment in Plants

In Ayurveda Chikungunya is known as Sandhijwara which literally means "fever of the

Symptoms of Chicken Pox

Following are the major chicken pox symptoms:

1. Low grade fever

Causes of Chicken Pox

Herbal Remedies for Chicken Pox

Material & Methods

MATERIALS AND METHODS

virus type I, strain KOS (University of Rennes/France), ATCC-VR733 and 29R-acyclovir

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