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HIV (Immunology (Cell Mediated Immunity (CD8 cytotoxic T cells play a role…
HIV
Immunology
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The resulting cell-mediated immunodeficiency leaves the host open to infection by viruses, bacteria, fungi, parasites and autoimmune disease
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There is a heterogenous group of individuals that never progress to AIDs. Their CD4 count remains >600 cells/ml
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B cells have enhanced activation and decreased proliferation - this lowers specific antibody production
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CD4 T cell depletion is caused by:
Impaired cell homeostasis
Apoptosis
Bystander cell killing
Decreased production
Infection of CD34+ progenitors in bone marrow
Pathophysiology
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HIV has reverse transcriptase to allow its RNA to be transcribed to DNA and incorporated into the host cell genome via integrase.
Reverse transcriptase is very error prone, leading to genetic variation in HIV:
Group M (major) - subtypes A-K
Group O (outlying)
Group N (new)
HIV enters via mucosa. Local infection is established within a mucosal macrophage and spreads to other antigen presenting cells which will present HIV antigen to T cells
HIV targets CD4 T cells. Interaction between CD4 and HIV glycoprotein gp120 with host chemokine co-receptor CCR5 is responsible for HIV entry into cells
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Due to CD4 T cell role in adaptive immune response, their depletion leads to AIDs: acquired immune deficiency syndrome
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Replication
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When infected cell divides, viral DNA is transcribed
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Treatment
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The drugs that form HAART include reverse transcriptase inhibitors, protease inhibitors, integrase inhibitors and fusion inhibitors
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There are 3+ drugs in HAART to combat resistance. The changes of mutations arising for all 3 drugs in one single virion is 0
Patient MUST adhere to drug regime. Drugs all have different half lives so if they are stopped, monotherapy will develop and resistance can occur
Drug interactions can cause resistance e.g. lansoprazole and clopidogrel cause lower therapeutic levels of antiretrovirals
Epidemiology
The sexual interaction that produces the greatest risk of acquiring HIV is receptive anal intercourse
Groups most at risk:
Men who have sex with men
Heterosexual women
IV drug users
Commercial sex workers
Heterosexual men
Truck drivers (they use sex industry more)
Migrant workers (they use sex industry more)
Uncircumcised men
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Transmission is via sexual contact, via contaminated blood, via contaminated needles in IV drug users who share needles and mother to child transmission perinatally or via breast milk and
Testing
Test for HIV when there is recurrent infection in an unexpected patient with no clear underlying cause
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Benefits of testing include reduction in morbidity and mortality, reduction in mother-child transmission, reduction of sexual transmission and it is cost-effective
Clinical Presentation
Acute HIV Syndrome
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Acute rise in viral load, then it falls to a set point
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Symptoms: Fever, sore throat, rash, vomiting, headache, lymphadenopathy, weight loss. If you see a patient with fever and rash - ask about sexual history
Clinical Latency
At first, immune system takes control and CD4 population increases and viral load decreases. However over time, CD4 population declines
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Early Symptomatic HIV
Symptoms:
Fever
Night sweats
Weight loss
Chronic diarrhoea
pportunistic infections e.g. shingles, oral candida, bacterial pneumonia, severe psoriasis
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AIDS
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Pneumocystis pneumonia is fungal. Fever, dry cough, pleuritic chest pain, drop in oxygen saturations after exertion
TB is an AIDs defining condition. All patients with TB require a HIV test. Presents with night sweats, weight loss, cough
HIV increases risk of getting any cancer associated with a virus: Karposi's sarcoma, non-Hodgkins lymphoma, invasive cervical carcinoma
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