RNA VIRUS ▪ Acite hemmorhagic conjunctivitis

▪ Hand-foot-and-mouth disease
▪ Aseptic meningitis
- COXSACKIE B VIRUS
▪ Pleurodynia (Bornholm disease, “devils
grip”)
o pain due to an infection of the
intercostal muscles (myositis), not
of the pleura
PICORNAVIRIDAE ▪ Severe generalized disease of infants
• POLIOVIRUS ▪ Myocarditis, pericarditis (most
➢ Morphology commonly identified causative agent of
- Naked (+) ssRNA heart disease in humans)
- Naked icosadheral symmetry ▪ Aseptic meningitis
- Three serologic (antigenic) types based on
different antigenic determinants on the • ECHO virus (Enteric CytopathicHuman Orphan)
outer capsid proteins ➢ Morphology: Naked (+) ssRNA
➢ Trans: Oral-fecal ➢ Trans: Oral-fecal
➢ Pathogenesis/Spectrum ➢ Pathogenesis/Spectrum
- Replicates in motor neurons in anterior horn - Aseptic meningitis
of SC, causing paralysis - Upper respiratory tract infection
- Host range is limited to primates - Febrile illness with and without rash
- Limitation is due to biding of the viral capsid - Infantile diarrhea
to a receptor found only on a primate cell - Hemorrhagic conjunctivitis
membrane ➢ Orphan virus means a virus that is not
➢ POLIOMYELITIS and MENINGITIS associated with any known disease
- Inapparent, asymptomatic infection
- ABORTIVE POLIOMYELITIS • RHINOVIRUS
▪ Most common ➢ Morphology
▪ Mild febrile illness with headache. Sore - Naked (+) ssRNA
throat, nausea, vomiting - more than 100 serotypes
- NON-PARALYTIC POLIOMYELITIS ➢ Trans: Aerosol droplets; hand-to-nose contact
▪ Aseptic meningitis ➢ Pathogenesis/Spectrum
- PARALYTIC POLIOMYELITIS - Replicate better at 33C than 37C
▪ Falccid paralysis, permanent nerve - Affect primarily the nose and conjunctiva
damage rather than the lower respiratory tract
➢ Diagnosis: COWDRY TYPE B INTRANUCLEAR - Acid-labile (killed by gastric acid when
INCLUSIONS swallowed)
➢ PREVENTION - Do not infect the GIT (unlike the enterovirus)
- SALK (IPV, Killed) - Host range limited to humans and
- SABIN (OPV, Live Attenuated) chimpanzees
▪ Preferred over Salk - COMMON COLD (most common infection)
▪ It interrupts fecal-oral transmission by
inducing secretory IgA in GIT • HEPATITIS A VIRUS (AKA ENTEROVIRUS72)
➢ Morphology
• COXSACKIE VIRUS - Naked (+) ssRNA
➢ Morphology - Has single serotype
- Naked (+) ssRNA ➢ Trans: Oral-fecal
- Classification is based on pathology in mice ➢ Pathogenesis/Spectrum
➢ Trans: Oral-fecal - Replicates in GI and then spreads to liver
➢ Pathogenesis/Spectrum during a brief viremic period
- COXSACKIE A VIRUS - Not cytopathic for the hepatocyte
▪ Hepangina (vesicular pharyngitis)

Page 1 of 12 | J.P. 2019

 - Hepatocellular injury is caused by immune - Rotavirus is resistant to stomach acid and
attack by cytotoxic T cells can reach the SI
- Children most frequently infected - villous destruction with atrophy – decrease
- Self-limited hepatitis absorption of Na and loss of K
- Short incubation hepatitis - VIRAL GASTROENTERITIS
- Anicteric hepatitis : asymptomatic or only ▪ Most common cause of childhood
mildly ill, absence of jaundice, with positive diaarhea
serologic evidence of infection ▪ Severe cause: stools are clear (white
➢ Diagnosis: Anti-HAV IgM (most useful for acute) stool diarrhea)
➢ Treatment: ➢ Treatment/Prevention
- Vaccine contains killed virus - ROTAVIRUS VACCINE
- Immne globulin during the incubation period ▪ 1st dose: 6wks of age
can mitigate the disease ▪ Last dose: not later than 32 wks of age
➢ Notes: no antigenic relationship between - MONOVALENT (RV1)/ROTARIX: 2 dose series
Hepatitis A and other Hepa virus - PENTAVALENT (RV5)/ROTATEQ: 3 dose
series
HERPESVIRIDAE - Min. interval : 4 weeks
• HEPATITIS E ➢ Notes
➢ Morphology: Naked icosahedral (+) ssRNA - SEGMENTED GENOME
➢ Trans: Oral-fecal ▪ Bunyavirus
➢ Pathogenesis/Spectrum ▪ Orthomyxovirus
- Causes outbreaks of hepatitis (epidemics) ▪ Arenavirus
- No chronic carrier state, no cirrhosis, no ▪ Reovirus
hepatocellular carcinoma
- Fulminant Hepatitis in pregnant woman ORTHOMYXOVIRIDAE
➢ Diagnosis • INFLUENZA VIRUS
- Liver Biopsy ➢ Morphology
- Patchy necrosis - Enveloped virus
➢ Notes: - Helical nucleocapsid
- Expectant (pregnant) mother - Segemented, ss-negative RNA
- Enteric ➢ Transmission: Respiratory Droplets
- Epidemic ➢ Pathogenesis/Spectrum
- INFLUENZA A
• NORWALK VIRUS (NOROVIRUS) ▪ These animal viruses are the source of
➢ Morphology: Naked icosahedral (+) ssRNA the RNA segments that encode the
➢ Trans: Oral-fecal antigenic shift variants that cause
➢ Pathogenesis/Spectrum epidemics among humans
- VIRAL GASTROENTERITIS ▪ Example: if an avian and a human
▪ Most impt cause of epidemic viral influenza A virus infect the same cell (in
(nonbacterial) gastroenteritis in adults a farmers respi tract) - REASSORTMENT
▪ Sudden onset of vomiting, diarrhea, - new variant of the human A virus,
accompanied by fever and abdominal bearing the avian hemagglutinin, may
cramping appear
▪ Aquatic birds (waterfowl)
• ROTAVIRUS o Common source of these new
➢ Morphology genes and that the reassortment
- Only RNA virus with a double-starnded RNA event leading to new human strains
genome occurs in pigs
- Naked double-layered capsid with ▪ Pigs may serve as the “mixing bowl”
segmented double stranded RNA (10 0r 11 within which the human, avian, and
segments) swine viruses reassort
➢ Pathogenesis/Spectrum ▪ Waterfowl : H1 to H6, N1 to N9
▪ Humans: H1 to H3, N1 and N2

Page 2 of 12 | J.P. 2019

 ▪ Worldwide epidemics (pandemics) o H. Influenzae
▪ 16 antigenically distinct types ▪ Reye’s Syndrome
hemmagglutinin ➢ Treatment/Prevention
▪ 9 antigenically distinct types of - Oseltamivir (DOC) and Zanamivir
neuraminidase - Neuraminidase inhibitors, which act by
- INFLUENZA B inhibiting the release of virus from infected
▪ Major outbreaks of influenza cells (for both influenza A and B)
▪ Does NOT lead to pandemic - Amantadine and Rimantidine (Influenza A;
▪ Is only a human virus no longer used due to widespread
▪ No animal source of new RNA segment resistance)
▪ Does not undergo antigenic shifts - Anual Vaccination (contain influenza A and
▪ Undergo enough antigenic drift that the B)
current strain must be included in the
new version of the influenza vaccine MNEMONICS
produced each year • POSITIVE-STRAND RNA VIRUS
▪ No antigens in common with influenza A “Call Pico Flavier To Call Astroboy Right away”
virus - Coronavirus
➢ Pathogenesis - Picornavirus
- Enveloped is covered with two different - Flavivirus
types of spikes (considered as the virus’ - Togavirus
major antigens) - Calicivirus
▪ HEMMAGGLUTININ - Astrovirus
o Bind to the cell surface receptor - Retrovirus
(neuraminic acid, sialic acid) to • NEGATIVE-STRAND RNA VIRUS
initiate infection of the cell “Always Bring Polymerase Or Fail Replication”
o Target of neutralizing antibody - Arenavirus
o Most important antigen - Bunyavirus
▪ NEURAMINIDASE - Paramyxovirus
o Cleaves neuraminic acid (sialic acid) - Orthomyxovirus
to release progeny virus from the - Filovirus
infected cell - Rhabdovirus
o Degrades the protective layer of
mucus in the respi tract - enhances PARAMYXOVIRIDAE
the ability of the virus to gain • MEASLES VIRUS
access to the respi epithelial cells ➢ Morphology
- Enveloped, helical, nonsegmented, ss-
negative
➢ Transmission: Respiratory Droplets

➢ Spectrum of disease ➢ Pathogenesis/Spectrum

- Incubation period: 24-48 hours - In chronological order:
- Fever, myalgia, headache, sore throat, cough ▪ Measles virus infects the cells lining the
- Complications: URT enters the blood
▪ Fatal bacterial superinfection ▪ Infects reticuloendothelial cells
o S. Aureus ▪ Spreads via the blood to the skin
o S. Pneumoniae

Page 3 of 12 | J.P. 2019

 ▪ Cytotoxic T-cells attack the measles ▪ Measles Active Vaccine can be given to
virus-infected vascular endothelial cells suscpetible children >1y/o within 72hrs
in the skin ➢ Notes
▪ Rash - Clinical manifestations of measles: (4C)
▪ Virus can no longer be recovered ▪ Cough
▪ Patient can no longer spread virus to ▪ Coryza
other ▪ Conjunctivitis
- Can transiently depress cell-mediated ▪ Coplik spots
immunity
- Infection confers lifelong immunity MNEMONICS
- Aka red measles, rubeola, “first disease” • PaRaMyxoviruses
- Incubation period: 10-14 days - Parainfluenza virus
- Period of communicability: 4 days before - RSV
and 4 days after the onset of rash - Measles
- Pathognomonic enanthem: - Mumps
▪ Koplik’s spots (bright red lesions with a
white central dot on the buccal mucosa) • MUMPS VIRUS
▪ Timing of appearance of rash: Height of ➢ Morphology
the fever - Enveloped, helical, nonsegmented, ss-
- Complications: negative
▪ Otitis media ➢ Transmission: Respiratory Droplets
▪ Giant cell Pneumonia, Secondary ➢ Pathogenesis/Spectrum
Bacterial Pneumonia
▪ Higher rate of activation of PTB
▪ Subacute Sclerosing Panencephalitis
(SSPE) / Dawson disease
o Neurodegenerative disease caused
by persistent infection of the brain
by an altered form of the measles
virus ➢ Treatment/Prevention
o Manifest 5-7yrs after initial - MMR vaccine
infection ▪ Live attenuated vaccine
- Final common pathway to a fatal outcome- ▪ Given SC
dev’t of: BRONHIOLOTIS OBLITERANS ▪ Diven at 15mos
➢ Diagnosis ▪ 2 doses recommended
- HP: Multinucleated giant cells ➢ Notes
(Warthin-Finkelday bodies) - 3 MCC of viral (aseptic) meningitis
➢ Treatment/Prevention ▪ Mumps virus
- Vitamin A supplementation ▪ Coxsackie virus
- Measles Vaccine ▪ Echovirus
▪ Live attenuated vaccine
▪ Subcutaneously • RESPIRATORY SYNCYTIAL VIRUS (RSV)
▪ Age: 9 months ➢ Morphology
▪ May be given as early as 6months of age - Enveloped, helical, nonsegmented, ss-
in cases of outbreaks negative
- MMR Vaccine ➢ Transmission:
▪ Subcutaneously - Respiratory Droplets
▪ Age: 15 months - Humans (natural hosts of RSV)
▪ 2 doses as recommended ➢ Pathogenesis/Spectrum
- Postexposure Prophylaxis - Surface spikes are fusion proteins, not
▪ Measles Ig for prevention and hemagglutinins or neuraminidase
attenuation within 6 days of exposure - Fusion protein causes cells to fuse, forming
multinucleated giant cells (syncytia)

Page 4 of 12 | J.P. 2019

 - VIRAL PNEUMONIA - When a human is bitten, the virus replicates
▪ RSV - most important cause of locally at the wound site for a few days
pneumonia and bronchiolitis in infants - Migrates (15-100mm/day) up to nerve axons
▪ Severe disease in infants due to to the CNS (retrograde transport)
immunologic cross-reactiob with
maternal antibodies
▪ RSV - impt cause of otitis media in
children and of pneumonia in the ederly
and in patients with chronic
cardiopulmonary diseases
➢ Treatment/Prevention
- Ribavirin
- Palivizumab (monoclonal antibody against F
protein)
▪ Prevents pneumonia caused by RSV
infection in premature infants

• PARAINFLUENZA VIRUS 1 and 2

➢ Morphology
- Enveloped, helical, nonsegmented, ss-
negative ➢ Diagnosis
➢ Transmission: Respiratory Droplets - HP: Negri bodies (cytoplasmic, round to oval,
➢ Pathogenesis/Spectrum eosinophilic inclusions
- LARYNGOTRACHEOBRONCHITIS / CROUP - Found in pyramidal neurons of the
▪ Results in “seal-like” barking cough and hippocampus and Purkije cells of the
inspiratory stridor cerebellum, sites usually devoid of
▪ Narrowing of upper trachea and inflammation
subglottis - steeple sign on x-ray - IMMUNOFLUORESCENT ANTIBODY TEST
▪ Severe croup can result in pulsus (IFAT) = gold standard detection
paradoxus secondary to upper airway ➢ Treatment/Prevention
obstruction - Pre-exposure:
- COMMON COLD ▪ Vaccine (PVRV or PDEV or PCEV - D0,
- PHARYNGITIS D7, and D21/28)
- LARYNGITIS - Post-exposure:
- OTITIS MEDIA ▪ Vaccine +/- Immunoglobulin
- BRONCHITIS
- PNEUMONIA
➢ Treatment/Prevention
- Racemic epinephrine

RHABDOVIRIDAE
• RABIES VIRUS
➢ Morphology
- Bullet-shaped
- Enveloped, helical, non segmented (-)ssRNA
➢ Transmission
- Animal reservoir: animal bite
▪ Dogs
▪ Cats
▪ Skunks FILOVIRIDAE
▪ Raccoons • EBOLA VIRUS
▪ Bats ➢ Morphology
➢ Pathogenesis/Spectrum - Enveloped, helical, non segmented, (-)ssRNA

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 - Thread-like virus
- Longest viruses
➢ Transmission
- Natural Host: fruit bats
(pteropodidae family)
- Direct contact with bodily fluids, fomites
(including dead bodies), infected bats or
primates (apes/monkeys)
➢ Pathogenesis/Spectrum
- Targets endothelial cells, phagocytes,
hepatocytes
- Incubation period: 2-21 days
- Abrupt onset of flu-like symptoms,
diarrhea/vomiting, high fever, myalgia
- Can progress to DIC, diffuse hemorrhage,
shock
- High mortality rate (100%)
➢ Diagnosis
- ELISA
- Antigen tests
- RT-PCR
➢ Treatment/Prevention
- Supportive care, no definitive treatment
- strict isolation
➢ Notes : Ebola virus is named for the river in
Zaire that was the site of an outbreak of
hemorrhagic fever in 1976
CORONAVIRIDAE
• CORONAVIRUS
➢ Morphology
- Enveloped, helical, non segmented, (+)ssRNA
- Thread-like virus
- Prominent clubshaped spikes form “corona”
(halo)
- 2 serotypes: 229E and OC43
➢ Transmission
- Respiratory droplet
- Reservoir: Horsedhoe bat
- Immediate host: Civet cat
➢ Pathogenesis/Spectrum
- COMMON COLDS
▪ 2nd to rhinovirus as the most common
cause of common colds
- SEVERE ACUTE RESPI SYNDROME
▪ Incubation period: 2-10days (mean,
5days)
▪ Receptor for SARS-CoV on surface of
cells is angiotensin-converting enzyme-2
(ACE-2)
▪ Binding of the virus to ACE-2 on the
surface of respi tract epithelium ->
dysregulation of fluid balnce -> alveolar
edema
▪ Severe atypical pneumonia rapidly
progressing to ARDS
▪ Leukopenia and thrombocytopenia
▪ CXR: interstitial “ground-glass”
infiltrates that do not cavitate
- MIDDLE EAST RESPI SYNDROME
▪ MERS-CoV binds to CD-26 on the
respiratory mucosa (not ACE-2)
▪ Clinical findings are similar to SARS
FLAVIVIRIDAE
• DENGUE VIRUS
➢ Morphology
- Enveloped, icosahedral, non segmented,
(+)ssRNA
- Four serotypes: (DEN-1,2,3,4)
- Each serotype provides specific lifetime
immunity
- Short term cross immunity
➢ Transmission
- Bite of female Aedes aegypti mosquito and
Aedes albopictus
- Aedes aegypti - recognized by white
markings on its legs and a marking in the
form of a lyre on the upper surface of its
thorax
➢ Pathogenesis/Spectrum
- DENGUE FEVER (BREAKBONE FEVER)
▪ Biphasic fever
▪ Myalgia
▪ Arthralgia
▪ Rash
▪ Leukopenia
▪ Lymphadenopathy
- DENGUE HEMORRHAGIC FEVER
▪ Capillary permeability
▪ Abnormalities of hemostasis
▪ Protein-losing shock syndrome
▪ Hemmorhagic shock syndrome
o Due to production of large
amounts of cross-reacting antibody
at the time of a second dengue
infection (antibody-dependent
enhancement)
➢ Diagnosis
- NS1 Antigen: to detect gene product (NS1
glycoprotein) from day 1 until day 6 from the
onset of fever
- RT-PCR: to detect dengue viral genes (RNA)
in acute phase serum samples which
coincide with the onset of viremia
Page 6 of 12 | J.P. 2019
 - Dengue IgM: marker of recent infection
- Dengue IgG: marker of past infection
- Fourfold increase confrims the diagnosis
- CBC-PC: Charateristic findings:
▪ Leukopenia
▪ Thrombocytopenia
▪ Hematocrit level increase >20% is a sig
of hemoconcentration and precedes
shock
➢ Treatment/Prevention
- Insecticides
- Draining stagnant water
- Mosquito repellent
- DENDVAXIA (CYD-TDV)
▪ First licensed in Mexico in December
2015 for use in individuals 9-45y/o
▪ Live recombinant
▪ Tetravalent dengue vaccine
▪ 3-dose series on a 0/6/12-month
schedule
➢ Notes: Dengue is the most common insect-
borne vioral disease in the world
• HEPATITIS C VIRUS
➢ Morphology
- Enveloped, icosahedral, non segmented,
(+)ssRNA
- Has at least 6 genotypes and multiple
subgenotypes based on differences in the
genes that encode one of its two envelope
glycoproteins
- The genetic variation results in a
“hypervariable” region in the envelope
glycoprotein
- Genotype 1: most common in US
➢ Transmission
- Humans are the reservoir for HCV
- HCV is the most prevalent bloodborne
pathogen in US
- MAJOR MODE OF TRANSMISSION:
▪ Blood-borne
▪ Setting: IV drug users
- MAJOR MODE OF TRANSMISSION:
▪ Needle-stick injury
▪ During birth
▪ Sexual
➢ Pathogenesis
- Replication of HCV in the liver enhanced by a
liver-specific micro-RNA called miR-122
- miR-122 acts by increasing the synthesis of
HCV mRNA
- Death of the hepatocytes is probably caused
by immune attack by cytotoxic T cells
- Alcoholism greatly enhances the rate of
hepatocellular carcinoma in HCV-infected
individuals
- Rate of chronic carriage of HCV is much
higher than that of HBV
➢ Spectrum of disease
- Incubation period: 8 weeks
- Acute infection: milder than HBV infection
- Hepatitis C resembles hepaB in ensuing:
▪ Chronic liver disease
▪ Cirrhosis
▪ Hepatocellular carcinoma
- HepaC leads to significant autoimmune
reactions and extrahepatic manifestations:
▪ Thyroiditis
▪ Autoimmune hemolytic anemia
▪ ITP
▪ MPGN
▪ Porphyria cutenea tarda
▪ DM
▪ Leukocytoclastic vasculitis
▪ Risk of B-cell NHL
▪ Lichen plannus
- HepaC main cause of essential mixed
cryoglobulinemia
➢ Diagnosis
- Anti-HCV antibodies: screening
- Recombinant immunoblot assay (RIBA):
confirmatory test
- PCR-based test
▪ Detects the presence of HCV-RNA (viral
load) in the serum
▪ Performed to determine whether active
disease exists
Page 7 of 12 | J.P. 2019
 ➢ Treatment/Prevention - Severe, life-threatening disease that begins
- ACUTE HEPATITIS C with the sudden onset of fever, headache,
▪ Peginterferon alfa myalgias and photophobia
- CHRONIC HEPATITIS C - After this prodrome, the symptoms progress
▪ Peginterferon alfa to involve the liver, heart and kidneys
▪ Ribavirin - Prostration and shock occur, accompanied
▪ Or combination by upper GI tract hemorrhage with
▪ If genotype 1, add: hematmesis (“black vomit”)
o Protease inhibitor (Boceprevir, ➢ Diagnosis
Simeprevir, Telaprevir) - Councilman bodies (eosinophili apoptotic
➢ Notes globules) on liver biopsy
- Cirrhosis resulting from chronic HCV ➢ Treatment/Prevention
infection - Mosquito control
- Most common indication for liver - Vaccine containing live, attenuated yello
transplantaion fever virus
- CHRONIC INFECTION is characterized:
▪ Elevated transaminase levels • WEST NILE VIRUS
▪ Positive RIBA ➢ Morphology
▪ Detectable viral RNA for at least 6mos - Enveloped, icosahedral, non segmented,
(+)ssRNA
• ZIKA VIRUS ➢ Transmission
➢ Morphology - Bite of Culex mosquito
- Enveloped, icosahedral, non segmented, - Reservoir: Wild Birds
(+)ssRNA - Humans are dead-end host
➢ Transmission ➢ Pathogenesis/Spectrum
- Aedes mosquito bites - Bird -mosquito-man cycle
- Sexual ▪ Virus transmitted via blood from bite
- Vertical transmission possible site to brain
➢ Pathogenesis/Spectrum - Initial self-limited febrile illness with
- Causes: progression to neuroinvasive disease
▪ Conjunctivitis - The most important picture is encephalitis
▪ Low-grade pyrexia with or without signs of meningitis (60y/0)
▪ Muscle and joint ▪ Asymptomatic in 80%
▪ Malaise ▪ Fever and headache in 20%
▪ Headache ▪ Encephalitis in 1%
▪ Itchy rash in 20% cases ➢ Notes
- Usually mild and last for 2-7days - Arbovirus is an acronym for arthropod-
- COMPLICATION: borne virus (mosquitoes and ticks)
▪ Microcephaly ▪ Togavirus
▪ Guillain-Barre Syndrome ▪ Flavivirus
➢ Treatment/Prevention ▪ Bunyavirus
- Supportive care
- No definitive treatment • JAPANESE B ENCEPHALITIS VIRUS
➢ Morphology
• YELLOW FEVER VIRUS - Enveloped, icosahedral, non segmented,
➢ Morphology (+)ssRNA
- Enveloped, icosahedral, non segmented, ➢ Transmission
(+)ssRNA - Bite of Culex mosquito
➢ Transmission - Prinicipal reservoir: Culex tritaeniorhynchus
- Reservoir: monkey or human summarosus
➢ Pathogenesis/Spectrum ➢ Pathogenesis/Spectrum
- JAUNDICE and FEVER - Most common cause of epidemic
encephalitis

Page 8 of 12 | J.P. 2019

 - Thalamic infarcts on CT Scan
➢ Treatment/Prevention
- JE VACCINE
▪ Live attenuated recombinant
monovalent viral vaccine
▪ Given 0.5ml subcutaneous for children
12 months and above
▪ Primary series: single dose
▪ Booster dose: 12-24 months after 1st
dose
TOGAVIRIDAE
• RUBELLA VIRUS
➢ Morphology
- Enveloped, icosahedral, non segmented,
(+)ssRNA
- Only one serotype
➢ Transmission
- Respiratory droplets
- Transplacentally
➢ Pathogenesis/Spectrum
- RUBELLA/GERMAN/3-DAY MEASLES
- Incubation period: 14-21 days
- Period of communicability: 1 week before up
to 1 week after the appearance of rash
- Prodrome: malaise, fever and anorexia for
several days; may be accompanied by mild
coryza and conjunctivitis (children may not
have a prodrome)
- Cephalocaudal appearance of maculopapular
rash
- Postauricular lymphadenopathy: most
characteristic clinical feature
- Enanthem: Forchheimer’s spots
▪ Petechiae on soft palate; not
pathognomonic
- Polyarthritis caused by immune complexes
(esp in adult women)
- Natural infection leads to lifelong immunity
- CONGENITAL RUBELLA SYNDROME
▪ Risk is greatest early in fetal
development when sell differentiation is
at peak (1st trimester)
▪ Rubivirus infected human embryo
demonstrate chromosomal breakage
and inhibition of mitosis
▪ Body ares affected:
o Heart: patent ductus,
interventricular septal defects,
pulmonary artery stenosis
o Eye: cataracts, chorioretinitis
oCNS: mental retardation,
microcephaly, sensorineural
deafness
▪ “Blueberry muffin” appearance due to
dermal extramedullary hematopoiesis
➢ Treatment/Prevention
- MMR VACCINE
▪ Live attenuated vaccine
▪ Given SC
▪ Given at 15mos
▪ 2 doses recommended
▪ Should not be given to
immunocompromised patients or to
pregnant women
MNEMONICS
• 5 Bs of CONGENITAL RUBELLA SYNDROME
- Bulag (cataracts)
- Bingi (SN deafness)
- Bobo (mental retardation)
- Butas puso (PDA)
- Blueberry muffin rash
RETROVIRIDAE
- Distinguished from all other RNA virus by the
presence of reverse transcriptase
- Converts a single starnded RNA viral genome
into a double-stranded viral DNA
- ssRNA -> dsDNA
• HUMAN IMMUNODEFICIENCY VIRUS (HIV)
➢ Morphology
- Enveloped virus with two copies (diploid) of
a single-stranded positive polarity RNA
genome
- Most complex of the known retroviruses
- Many serotypes
➢ Structure
- Transmembrane protein (fusion protein,
also called gp41) - linked to a serface
protein, and SU (attachment protein, gp120)
- Cone-shaped, icosahedral core containing
the major capsid protein (CA also called
p24)
- MA (outer matrix protein, p17) - directs
entry of the doublestranded DNA provirus
into the nucleus, and is later essential for the
process of virus assembly
- There are two identical copies of the positive
sense, single-stranded RNA genome in the
capsid (that is, unlike other virus,
retroviruses are diploid)
Page 9 of 12 | J.P. 2019
- The RNA is tightly complexed with a basic
protein NC
- NC (nucleoprotein, p7) in a nucleocapsid
structure in morphology among the different
retrovirus genera
- P24
▪ Group-specific antigen
▪ Located in the core
▪ Not known to vary
▪ Antibodies against p24 do not neutralize
HIV infectivity but serve as important
serologic markers of infection
- Gp120
▪ Interacts with the CD4 receptor
▪ Gene mutates rapidly - many antigenic
variants
▪ V3 loop: most immunologic region of
gp120
▪ Antibody neutralized HIV infectivity, but
the rapid appearance of variants -
difficult to prepare vaccine
▪ High mutation rate may be due to lack
of an editing function in the reverse
transcriptase
- Gp41
▪ Mediates the fusion of the viral
envelope with the cell membrane at the
time of infection
➢ Transmission
- Original source: chimpanzees
- Transfer of body fluids
- Transplacental
- Perinatal
- needlestick
➢ Pathogenesis/Spectrum
- Virus binds to CD4 as well as coreceptor,
either:
▪ CCR5 on macrophages (early infection)
▪ CXCR4 on T cells (late infection)
- MARAVIROC is a CCR5 receptor antagonist
- Pereferentially infects and kills helper (CD4+)
T lymphocytes:
▪ Loss of cell-mediated immunity
▪ High probability of opportunistic
infections
- Main immune response consists of cytotoxic
(CD8+) lymphocytes
- Also targets a subset of CD4+ cells called
Th17 cells, which are impt mediator of
mucosal immunity:
▪ Th17 cells produce IL-17, which attracts
meutrophils to the site of bacterial
infection
▪ Loss of Th17 cells a bloodstream
infectiobs by bacteria in the normal
flora of the colon (E. coli)
Page 10 of 12 | J.P. 2019

➢ Diagnosis
- Presumptive diagnosis:
▪ Detection of antibodies in the patients
serum to the p24 protein of HIV using
ELISA
▪ There are some false-positive results
with this test
- Definitive diagnosis: WESTERN BLOT
(IMMUNOBLOT) ANALYSIS
▪ Viral proteins are displayed by
acrylamide gel electrophoresis,
transferred to nitrocellulose paper (the
blot), and reacted with the patients
serum
▪ If antibodies are present in the patients
serum, they will bind to the viral
proteins (predominantly to the gp41 or
p24 protein)
▪ Enzymatically labeled antibody to
human IgG is then added
▪ A color reaction reveals the presence of
the HIV antbiody in the infected
patients serum
- PCR
▪ Very sensitive and specific technique
▪ Detect HIV DNA within infected cells
▪Amount of viral RNA in the plasma (viral
load) can also be determine using PCR-
based assays
➢ Treatment
- HIGHLY ACTIVE ANTIRETROVIRAL THERAPY
(HAART)
▪ Strongest indication for patients
presenting with:
o AIDS-defining illness
o Low CD4+ cell counts (<500
cells/mm3)
o High viral load
▪ Regimen consists of 3 drugs to prevent
resistance: 2NRTIs + Protease inhibitor
o Zidovudine, Lamivudine (NRTI)
o Indinavir (PI)
- IMMUNE RECONSTITUTION INFLAMMATORY
SYNDROME (IRIS)
▪ Collection of inflammatory disorders
associated with paradoxical worsening
of preexisting infectious processes (HBV,
HCV, MAC, MAI) following the initiation
HAART in HIV-infected individuals
➢ Prevention
- General prevention:
▪ Condoms
▪ Not sharing needles
▪ Proper blood disposal
▪ Postexposure prophylaxis
- Perinatal prevention:
▪ Perinatal prophylaxis
▪ Cesarean delivery
▪ Breastfeeding cessation
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