FAMILY:
These areRNA viruses that belong to family
retroviridae.
Members of this family possess reverse
transcriptase enzyme which prepares a DNA
copy of the RNA genome in host cell.
3.
MORPHOLOGY:
HIV isa spherical enveloped virus, about 90-120 nm
in diameter.
It contains two identical copies of single stranded
RNA genome.
The virus core is surrounded by a nucleocapsid
composed of protein.
The virus contains a lipoprotein envelope and
glycoproteins.
4.
VIRAL GENES ANDANTIGEN
HIV genome contains the three structural
genes;
1) gag gene
2) pol gene
3) env gene
The products of these genes, both structural
and non-structural, act as antigens.
5.
GENES CODING FOR
STRUCTURALPROTEINS
1) The gag gene:
The gag gene codes for the core and
shell of the virus.
It is expressed as a precursor
protein, p55 which is cleaved into
three proteins,
p17 constitutes the matrix or shell
antigen , p24 and p15- constitute
the core antigens
6.
2)The pol gene
Thepol gene codes for viral enzymes
such as reverse transcriptase,
protease and integrase.
3)The env gene
The env gene codes for the envelope
glycoprotein which is cleaved into
two components:
gp 120: it is the main receptor of HIV
that binds to CD4 molecules on host
cell to initiate infection.
gp41
7.
MODE OF TRANSMISSION
Sexualmode
It is by far the most common mode
of transmission, accounts for 75% of
total cases in the world.
Heterosexual route (male to female
via vaginal coitus) is the commonest
mode.
Anal intercourse (among homosexual
males or even male to female) has
higher risk of transmission than
vaginal intercourse.
8.
Blood transfusion, thoughis the
least common mode of transmission
(5%) but the risk of transmission
ismaximwn (90- 95%).
Percuraneous/mucosal transmission
modes such as needle stick injury,
injection drug abuse and sharing
razors or tatooing or splashes of
infected blood on eyes etc. are
among the less effective modes of
transmission.
9.
Perinatal mode:
In theabsence of any intervention,
the risk of transmission from mother
to fetus is about 20-40%.
Transmission may occur at any time
during pregancy and breast feeding
but the risk is maximum during
delivery.
Risk is maximum if mother is
recently infected or has already
developed AIDS.
10.
PATHOGENESIS
HIV enters intothe target cells by
binding its gp 120 to the CD4
receptor on host cell surface.
CD4 molecules are mainly expressed
on helper T cells; and also on the
surface of various other cells like
monocytes, macrophages,
Langerhans cells.
11.
A second co-receptorin addition to
CD4 is necessary for fusion of HIV to
gain entry into the host cell.
Usually, the chemokine receptors act
as co-receptors for HIV and act by
binding to gp120. Examples include:
CCR5
12.
Fusion: Following attachmentof
receptor and co-receptor to gp 120,
fusion of HIV to host cell takes
place.
Penetration and uncoating: After
fusion, HIV nucleocapsid enters into
the host cell cytoplasm,which is
followed by uncoating and release of
two copies of ssRNA and viral
enzymes.
13.
Reverse transcription:
Viral reversetranscriptase mediates
transcription of its ssRNA into ssDNA
so that DNA-RNA hybrid is formed.
The RNA is degraded by viral
endonuclease and ssDNA replicates
to form ds DNA.
14.
Integration:
The viral dsDNAgets integrated into
the host cell chromosome; mediated
by viral integrase. The integrated
virus is called as provirus.
Latency:
In the integrated state, HIV
establishes a latent infection for
variable period.
15.
CLINICAL FEATURES
AIDS isthe last stage in the wide
spectrum of clinical features in HIV
infection.
The Centers for Disease Control and
Prevention, USA, have classified the
clinical course of HIV infection under
various groups;
16.
Group I- AcuteHIV infection:
Within 3- 6 weeks of infection with
HIV, about 50 percent of persons
experience low-grade fever,
malaise, headache,
lymphadenopathy, sometimes with
rash.
Rarely, there may be acute
encephalopathy. Spontaneous
resolution occurs within weeks.
17.
Seroconversion illness:
Tests forHIV antibodies are usually
negative at the onset of the illness
but become positive during its
course, though in many of those
infected there may not be any
apparent clinical illness.
18.
Group II- asymptomaticor latent
infection:
All persons infected with HIV,
whether or not they experience
seroconversion illness, pass through
a phase of symptomless infection
(clinical latency) which may last up
to several years.
They are positive for HIV antibody
and are infectious.
19.
The median timebetween primary
HIV infection and the development
of AIDS has been stated as
approximately 10 years.
The host mounts an immune
response against the virus, both
humoral and cellular, which can only
limit the virus load, but not clear it
completely.
20.
Group III-persistent generalised
lymphadenopathy(PGL):
This has been defined as the
presence of enlarged lymph nodes,
in two or more non-contiguous
extrainguinal sites, that persist for
at least three months.
21.
Group IV-AIDS-related complex
(ARC):
Thetypical constitutional symptoms
are fatigue, unexplained fever,
persistent diarrhea and marked
weight loss of more than 10 per cent
of body weight.
The common opportunistic infections
are oral and esophageal candidosis,
herpes zoster, salmonellosis or
tuberculosis.
Generalised lymphadenopathy and
splenomegaly are usually present.
22.
AIDS: This isthe end-stage disease,
representing the irreversible
breakdown of immune defence
mechanisms leaving the patient
open to progressive opportunistic
infections and malignancies
23.
Respiratory symptoms:
The commonestpresentation is dry
cough, dyspnea and fever. In
developing countries including India,
the most important pathogen is
M.tuberculosis.
Pneumonia may be viral (CMV) or
fungal.
24.
Gastrointestinal system:
Oral thrush,herpetic stomatitis,
gingivitis, leukoplakia or Kaposi's
sarcoma are common oral
manifestations.
Dysphagia may be due to esophageal
candidosis.
25.
Central nervous system:
Thetypical CNS opportunistic
infections are toxoplasmosis.
Infections are also seen with CMV,
herpes
simplex, mycobacteria, aspergillus
and candida.
Lymphomas of the central nervous
system are common.