HIV/AIDS and
principles of ART
Lechamo
• HIV is the etiologic
agent of AIDS;
• HIV1
• HIV2
• Virus infect
immune cell
resulting in
immune deficiency
of the host.
pathogenesis
Progression to chronic
immunodeficiency
•HIV infects CD4+ lymphocytes, then reproduces and spreads
to other CD4+ lymphocytes near the original site of infection →
infection of CD4+ lymphocytes concentrated in specialized
lymphoid tissue (e.g., lymph nodes or gut-associated
lymphatic tissue (GALT) ) → explosive growth and
dissemination → acute HIV syndrome with high viral load
•Window period: The time between infection and detectability
of HIV antibodies.
•After the acute stage, viral load decreases and remains at
roughly that level for approximately 8–10 years (clinical
latency stage ).
•During the clinical latency phase, the virus mainly
replicates inside the lymph nodes.
•Increasing loss of CD4+ lymphocytes impairs
immune function and, thereby, facilitates
opportunistic infections and development of
malignancies (AIDS). These secondary diseases
are usually the cause of death in individuals with
HIV.
•Increased viral load generally leads to a decreased
number of CD4+ lymphocytes and vice versa, but
the relation is not linear.
• Viral load predicts the rate of disease progression
and CD4 count correlates with immune function.
Clinical features
There are no clinical features specific to HIV
infection
•In early HIV infection, patients are often
asymptomatic.
•Incubation period: usually 2–4 weeks
•[12]
•Infectiousness: two peaks (1st peak: within the
first months after infection; 2 nd peak: during AIDS
-stage)
Acute HIV infection
•Also referred to as acute retroviral syndrome (ARS)
or described as a mononucleosis-like syndrome
•Fever
•Fatigue
•Myalgia and arthralgia
•Headache
•Generalized nontender lymphadenopathy
•Generalized rash
•Gastrointestinal symptoms (nausea, diarrhea, weight loss)
•Oropharyngeal symptoms (sore throat, ulcerations, painful
swallowing)
Clinical latency and
AIDS
• Clinical latency: Infected individuals may still be asymptomatic.
• Non-AIDS-defining conditions (common when CD4+ count is below
500 cells/mm3)
• Chronic subfebrile temperatures
• Persistent generalized lymphadenopathy
• Chronic diarrhea (> 1 month)
• Localized opportunistic infections
• Oral candidiasis: creamy, white patches on the mucous membranes of the mouth
that can be scraped off
• Vaginal infections (e.g., yeast, trichomonads)
• Oral hairy leukoplakia: lesions that cannot be scraped off located mainly
on the lateral borders of the tongue; triggered by Epstein-Barr virus
• HPV-related: squamous cell carcinoma of the anus (common in men who
have sex with men) or cervix
• Skin manifestations (e.g. molluscum contagiosum, warts, exacerbations
of psoriasis, shingles)
AIDS-defining conditions
•a set of potentially life-threatening conditions that indicate
the progression of HIV infection to AIDS
•As the CD4 count declines, the immune system is
weakened and many pathological processes may occur,
such as:
•Development of malignancies e.g., non-Hodgkin lymphomas
•Rapid spread of opportunistic and nonopportunistic bacterial
and fungal infections (e.g., coccidioidomycosis,
pneumocystis pneumonia, mycobacterial infections)
•Reactivation of latent infections (e.g., tuberculosis, herpes
simplex infections, shingles)
•AIDS (also known as advanced HIV) is defined as the
development of an AIDS-defining condition or a CD4 count
of < 200 cells/μL in HIV-infected patients.
Diagnosis
• Serologic tests
• both screening and diagnosis and may detect HIV
antigen, antibodies, or both.
• Virological testing
• Virological tests are most commonly used for
screening infants and confirmation of disease in
both infants and adults.
• CD4+ count: correlates with overall immune function
• Normal values are > 500 cells/mm 3, whereas in the
advanced stages of HIV the CD4+ count is often < 200
cells/mm3.
• Critical measurement to determine when to initiate
opportunistic infection prophylaxis
• CD4+ counts increase in response to successful ART
therapy.
•Viral RNA load: indicator of ART response
•Decrease in viral loads indicates effective treatment.
•Prognostic marker in long-term treatment (higher viral load
→ ↑ destruction of CD4+ lymphocytes → more severe
immunodeficiency → worse prognosis)
Management: General
principles
•Antiretroviral therapy
•All individuals with HIV infection, regardless of
CD4 count, should begin antiretroviral therapy (ART)
as soon as possible
•Antiretroviral drugs are combined to prevent
resistance.
•All antiretroviral drugs are able to target both HIV-1
and HIV-2, except for enfuvirtide and NNRTIs.
•Establish regular monitoring to assess treatment
response.
•Prevention and management of co-infections and
complications
•Screen patients for STIs and common opportunistic infections (see
“Diagnosis”).
•If CD4 count is < 200, start prophylaxis for opportunistic infections.
•Primary preventive measures (e.g., vaccinations, cancer screening)
•Prevention of onward transmission
•Counsel patients on safe sex practices
•Offer HIV testing for family or sexual partners.
•Referral to needle exchange programs and opioid substitution therapy
•Report infections to the appropriate health department based on local
guidance.
•Counseling and psychosocial support
•Provide counseling regarding diagnosis and management
•Multidisciplinary management recommended
