Hiv Aids 1

Acquired Immunodeficiency
Syndrome (AIDS)
By:
Dr: Manhal AbdulGadir
MBBS U of K
MD clinical pathology U of K
MHPE SMSB
HIV
• HIV is a nontransforming human retrovirus
belonging to the lentivirus family
• HIV-1 and HIV-2, genetically different but
related forms.HIV-1 is the most common type
associated with AIDS in the US, Europe, and
Central Africa
• HIV-2 causes a similar disease principally in
West Africa and India
Structure of HIV
• spherical and contains an electron-dense, cone-
shaped core surrounded by a lipid envelope
• The virus core contains
(1) the major capsid protein p24
(2) nucleocapsid protein p7/p9
(3) two copies of viral genomic RNA
(4) the three viral enzymes (protease, reverse
transcriptase, and integrase).
• core is surrounded by a matrix protein p17
• Studding the envelope are two viral
glycoproteins, gp120 and gp41
Acquired Immunodeficiency Syndrome AIDS:
Is a retroviral disease caused by the human
immunodeficiency virus (HIV).
It is characterized by infection and depletion of CD4+ T
lymphocytes, and by profound immunosuppression
leading to opportunistic infections, secondary
neoplasms, and neurologic manifestations.
AIDS represents the fifth most common cause of death
in adults between the ages of 25 and 44 years.
Transmission
• occurs under conditions that facilitate
exchange of blood or body fluids containing
thevirus or virus-infected cells. The three
major routes of transmission are sexual
contact, parenteral inoculation, and passage
of the virus from infected mothers to their
newborn
Pathogenesis of HIV
• The life cycle of HIV consists of infection of
cells, integration of the provirus into the host
cell genome, activation of viral replication,
and production and release of infectious
virus
• HIV infects cells by using the CD4 molecule as
a receptor and various chemokine (CCR5 and
CXCR4) receptors as co-receptors
• Once internalized, the RNA genome of the
virus undergoes reverse transcription, leading
to the synthesis of double-stranded
complementary DNA integration
the provirus may be silent for months or years,
a form of latent infection
• Completion of the viral life cycle in latently
infected cells occurs only after cell activation,
and in the case of most CD4+ T cells, virus
activation results in death of the infected cells.
Loss of CD4+ T cells
• T cell death during viral replication and budding: due
to interference with normal host cell protein synthesis
or to increased membrane permeability associated
with viral budding
• Apoptosis occurring as a result of chronic stimulation;
• Decreased thymic output;
• Functional defects
• Defective macrophage and DC functions
• Destruction of architecture of lymphoid tissues (late)
Natural History and Course of HIV Infection
• Acute phase: Primary infection, virus

dissemination, and the acute retroviral
syndrome is characterized by transient
viremia, widespread seeding of mucosal
lymphoid tissue and infection of memory T
cells, a temporary fall in CD4+ T cells, followed
by antibody seroconversion and generation of
CD8+ antiviral T cells.
• Clinically, a self-limited acute illness occurs in
40% to 90% of infected individuals with sore
throat, fatigue, myalgias, fever, rash,
adenopathy, and/or weight loss. Clinical
improvement and a partial recovery in CD4þ T-
cell counts occur within 6 to 12 weeks.
• Chronic phase: Chronic infection is
characterized by clinical latency (absence of
symptoms) despite ongoing vigorous viral
replication; lymph nodes and spleen are the
major sites of viral production.
• The period of clinical latency is typically 7 to
10 years in untreated patients
• AIDS. The final phase is progression to AIDS,
characterized by a breakdown of host defense,
a dramatic increase in plasma virus, and
severe, life-threatening clinical disease.
• The extent of viremia, measured as HIV-1
RNA levels in the blood, is a useful marker of
HIV disease progression and is of value in the
management of HIV-infected individuals
Clinical Features:
The clinical manifestations of HIV infection range

from a mild acute illness to severe disease.
Patient with AIDS presents with fever, weight
loss, diarrhea, generalized lymphadenopathy,
multiple opportunistic infections, neurologic
disease, and (in many cases) secondary
neoplasms.
AIDS-Defining Opportunistic Infections and Neoplasms
Found in Patients with HIV Infection:
(1) Infections :
PROTOZOAL AND HELMINTHIC INFECTIONS
Cryptosporidiosis or isosporidiosis (enteritis)
Pneumocystosis (pneumonia or disseminated infection)
Toxoplasmosis (pneumonia or CNS infection)
FUNGAL INFECTIONS
Candidiasis (esophageal, tracheal, or pulmonary)
Cryptococcosis (CNS infection)
Coccidioidomycosis (disseminated)
Histoplasmosis (disseminated)
BACTERIAL INFECTIONS
Mycobacteriosis ("atypical," e.g., Mycobacterium avium-
intracellulare, disseminated or extrapulmonary; M.tuberculosis,
pulmonary or extrapulmonary)
Nocardiosis (pneumonia, meningitis, disseminated)
Salmonella infections, disseminated
VIRAL INFECTIONS
Cytogegalovirus (pulmonary, intestinal, retinitis, or CNS
infections)
Herpes simplex virus (localized or disseminated)
Varicella-zoster virus (localized or disseminated)
Progressive multifocal leukoencephalopathy
(2)Neoplasms:
Kaposi sacroma
Non-Hodgkin lymphomas (Burkitt,
immunoblastic)
Primary lymphoma of brain
Invasive cancer of uterine cervix
anal cancer
Central Nervous System Disease
Viral meningoencephalitis
Aseptic meningitis
Vacuolar myelopathy
Peripheral neuropathies
Progressive encephalopathy called HIV-
associated neurocognitive disorder
THANK YOU

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Acquired Immunodeficiency

• Acute phase: Primary infection, virus

The clinical manifestations of HIV infection range

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