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Human immunodeficiency virus (HIV) (Pathophysiology (Life cycle (Entry…

- - - - Definition
        Asymptomatic for many years
      - Clinical presentation
        Asymptomatic
        Persistent generalised lymphadenopathy
      - Timing
        Lasts ~8y (w/o treatment)
    - - Timing
        ~8y after infection (w/o treatment)
      - Clinical presentation
        Constitutional: fever, night sweats, weight loss, diarrhoea
        Opportunistic infections: candida, oral hairy leukoplakia, herpes zoster, HSV, seberrhoic dermatitis, tinea
      - Definition
        Prodrome to AIDS
      - Pathophysiology
        Increased viral load and reduced CD4+ cells
    - - Timing
        Transient illness 2-6wk after, lasts 1-3wk
      - Pathophysiology
        Seroconversion to HIV+ Abs
      - Definition
        Acute/primary infection
      - Clinical presentation
        Malaise, fever, myalgia, pharyngitis, maculopapular rash
    - - Timing
        ~10y from infection (w/o treatment)
        ~2 years after onset of ARC
        Death <2y AIDS onset
      - Indicator
        diseases
        
        Cancer
        Cervical ca, Kaposi's sarcoma, Burkitt's lymphoma,
        CNS lymphoma
        
        Wasting syndrome
        Weight loss, muscle wasting
        
        Infection
        Fungal: candida, coccidomycosis, cryptococcus, histoplasmosis, Viral: CMV, HSV, PML, HIV encephalopathy
        Bacterial: TB, MAI, PCP
        Parasitic: toxoplasmosis
      - Definition
        Severe immunosuppression (CD4+ <200)
        HIV+ plus an indicator disease
- - - - Nucleoside/tide reverse transcriptase inhibitors (NRTIs)
        E.g. zidovudine, tenofovir
        MOA: inhibit RT by acting as substitute for nucleotides, preventing formation of a DNA copy of viral genome
        SEs: GIT, liver toxicity/hepatitis, anaemia, fever, rash, myalgia, pancreatitis, neuropathy, lipodystrophy
        Interactions: MANY drugs (CYP450)
      - Non-nucleotide reverse transcriptase inhibitors (NNRTIs)
        E.g. efavirenz, nevirapine
        MOA: inhibit RT directly by binding and preventing DNA copy
        SEs: SJS, TEN, hepatitis, rash
      - Protease inhibitors (PIs)
        E.g. lopinavir, ritonavir
        MOA: inhibit protease, preventing formation of new virions
        SEs: dyslipidemia, hyperglycaemia, DM, myalgia, rash, ulcers
        Interactions: MANY (due to CYP450 interactions)
      - Integrase inhibitors (IIs)
        E.g. raltegravir
        MOA: inhibit integrase, preventing
        integration of viral DNA into host genome
        SEs: GIT, insomnia
      - Fusion inhibitors
        E.g. infuvertide
        MOA: bind to envelope proteins, preventing fusion to and infection of CD4+ immune cells
      - CCR5 antagonists
        E.g. miraviroc
        MOA: bind CCR5, preventing initial infection of cells