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AIDS

Epidemiology of HIV/AIDS
AIDS was first recognised in 1981
2
nd
leading cause of disease burden worldwide and leading cause of
death in Africa.
HIV continues to be a major global public health issue, having claimed
more than 25 million lives over the past three decades.
There were approximately 34 [31.435.9] million people living with HIV in
2011.
Sub-Saharan Africa is the most affected region, with nearly 1 in every 20
adults living with HIV. 69 %of all people living with HIV are living in this
region.
HIV infection is usually diagnosed through blood tests detecting the
presence or absence of HIV antibodies.
There is no cure for HIV infection. However, effective treatment with
antiretroviral drugs can control the virus so that people with HIV can
enjoy healthy and productive lives.
In 2012, more than 9.7 million people living with HIV were receiving
antiretroviral therapy (ART) in low- and middle-income countries.

DEFINITION AND CLINICAL CLASSIFICATION OF HIV
INFECTION AND AIDS
HIV infection is defined as the stage when an
individual is infected by HIV, indicated by the
presence of anti HIV antibody and/or HIV P24
antigen in the serum confirmed by a designated
Reference Laboratory.

AIDS is defined as when an individual has the anti
HIV antibody confirmed to be positive as above and
in addition has at least one of the AIDS defining
conditions and CD4 T cells lymphocyte count of less
than 200/ml.
HIV


Human immunodeficiency virus (HIV) is
a lentivirus (slowly replicating retrovirus) that
causes acquired immunodeficiency syndrome (AIDS).
Two types of HIV have been characterized: HIV-1 and
HIV-2. HIV-1 is the virus that was initially discovered
and termed both LAV and HTLV-III. It is more virulent,
more infective, and is the cause of the majority of HIV
infections globally. The lower infectivity of HIV-2
compared to HIV-1 implies that fewer of those exposed
to HIV-2 will be infected per exposure.

LIFE CYCLE OF HIV
STAGE1:Engagement of the viral gp120 and the CD4 cell receptor
which results in a conformational change in gp120.
STAGE 2:This permits interaction with one of two chemokine co-
receptors (CXCR4 or CCR5)
STAGE 3: membrane fusion and cellular entry involving gp41
LIFE CYCLE OF HIV
STAGE 4:After penetrating the cell and uncoating, a DNA copy is transcribed
from the RNA genome by the reverse transcriptase (RT) enzyme
STAGE 5:This DNA is transported into the nucleus and integrated randomly
within the host cell genome via integrase enzyme . Integrated virus is known
as proviral DNA.
STAGE 6:On host-cell activation, this DNA copy is used as a template to
transcribe new RNA copies , which are processed and exported from the
nucleus
LIFE CYCLE OF HIV
STAGE 7:viral mRNA then being translated into viral peptide chains .
STAGE 8:The precursor polyproteins are then cleaved by the viral
protease enzyme to form new viral structural proteins and viral
enzymes such as the reverse transcriptase and protease. These then
migrate to the cell surface and are assembled using the host cellular
apparatus to produce infectious viral particles.
STAGE 9:These bud from the cell surface, incorporating the host cell
membrane as their own lipid bilayer coat, and cell lysis occurs . Once
maturation is complete, the new infectious virus (virion) is then
available to infect uninfected cells and repeat the process.

Primary infection
symptomatic in 7080% of cases and usually occurs 26 weeks after exposure. This
coincides with high plasma HIV-RNA levels and a fall in the CD4 count to 300400
cells/mm3, but occasionally to below 200 when opportunistic infections (e.g.
oropharyngeal candidiasis, Pneumocystis jirovecii pneumonia (PCP)) may rarely
occur. Symptomatic recovery parallels the return of the CD4 count (although this
rarely recovers to its previous value) and fall in the viral load. In many patients, the
illness is mild and only identified on retrospective enquiry at later presentation.
Diagnosis is made by detecting HIV-RNA in the serum or by immunoblot assay .
The appearance of specific anti-HIV antibodies in serum (seroconversion) takes
place later at 312 weeks (median 8 weeks).

Clinical features of primary infection
Fever with rashes
Pharyngitis with cervical lymphadenopathy
Myalgia/arthralgia
Headache
Mucosal ulceration
Asymptomatic infection (category A disease in the Centers for
Disease Control (CDC) classification)
follows and lasts for a variable period, during which the infected individual
remains well with no evidence of disease except for the possible presence of
persistent generalised lymph adenopathy (PGL, defined as enlarged glands at
more than 2 extra-inguinal sites).
At this stage the bulk of virus replication takes place within lymphoid tissue
(e.g. follicular dendritic cells).
There is sustained viraemia with a decline in CD4 count dependent on the
height of the viral load but usually between 50 and 150 cells/year .

Mildly symptomatic disease (CDC classification category B
disease)
develops in the majority, indicating some impairment of cellular immunity
but which is not AIDS-defining . The median interval from infection to the
development of symptoms is around 710 years, although subgroups of
patients exhibit fast or slow rates of progression.

AIDS (CDC classification category C disease)
defined by the development of specified opportunistic infections, tumours
and presentations

MODES OF TRANSMISSION
TRANSMISSION RISK AFTER EXPOSURE
EXPOSURE ROUTES CHANCE OF INFECTION(%)
BLOOD/BLOOD PRODUCTS >90
VERTICAL ROUTE 15-40
INJECTION DRUG USE 0.5-1.0
GENITAL MUCOUS MEMBRANCE SPREAD 0.2-0.5
NON-GENITAL MUCOSAL MEMBRANCE
SPREAD
0.1

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