HIV co-infections (HBV, HCV, TB)

HIV co-infections (HBV, HCV, TB)

HIV co-infections (HBV, HCV, TB)

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HIV-HBV Co-infection - Double Trouble Diagnosis

  • Universal Screening: All HIV-positive individuals require HBV screening at initial diagnosis.
  • Initial Serology Panel:
    • HBsAg (Hepatitis B surface antigen)
    • anti-HBs (Hepatitis B surface antibody)
    • anti-HBc (Total hepatitis B core antibody)
  • Key Interpretations:
    • HBsAg (+): Active HBV infection.
    • anti-HBs (+) & anti-HBc (+/-): Immune (natural infection or vaccination).
    • Isolated anti-HBc (+): May indicate occult infection; check HBV DNA.

⭐ HIV infection significantly accelerates liver fibrosis progression in patients with chronic HBV, increasing the risk of cirrhosis and hepatocellular carcinoma by 3-6x.

HIV-HCV Co-infection - The Liver's Other Foe

  • Epidemiology: Affects ~25% of HIV+ individuals, especially people who inject drugs (PWID). HIV co-infection increases the risk of chronic HCV to >80%.
  • Pathophysiology: HIV accelerates HCV progression by impairing HCV-specific T-cell immunity.
    • This leads to faster liver fibrosis, earlier onset of cirrhosis, and a higher risk of hepatocellular carcinoma (HCC).
    • HCV itself does not accelerate HIV progression.
  • Management:
    • Screen all HIV+ patients with an HCV antibody test; if positive, confirm with an HCV RNA viral load.
    • Initiate antiretroviral therapy (ART) for HIV first.
    • Once HIV is virologically suppressed, treat HCV with Direct-Acting Antivirals (DAAs), achieving >95% cure rates.
    • ⚠️ Monitor for drug-drug interactions between ART and DAAs.

⭐ In co-infected patients on effective ART, liver disease (cirrhosis, ESLD) surpasses AIDS-defining illnesses as a leading cause of mortality.

HIV-TB Co-infection - The Lethal Alliance

  • HIV is the most potent risk factor for reactivating latent Mycobacterium tuberculosis (MTB), increasing annual risk from 5-10% (lifetime) to 5-10% (annually).
  • Clinical presentation is stratified by CD4 count:
    • CD4 >200 cells/μL: Classic upper-lobe cavitary pulmonary TB.
    • CD4 <200 cells/μL: Atypical patterns; extrapulmonary disease (lymphadenitis, meningitis) and disseminated/miliary TB are common. Chest X-rays can be normal.

Chest X-ray: Miliary TB in HIV-positive patient

  • Diagnosis: Tuberculin skin tests (TST) are unreliable due to anergy; Interferon-Gamma Release Assays (IGRAs) are preferred for latent TB. For active TB, nucleic acid amplification tests (NAAT) like Xpert MTB/RIF on sputum are crucial due to paucibacillary disease.

⭐ Paradoxical worsening of TB symptoms after starting antiretroviral therapy (ART) is the hallmark of TB-Immune Reconstitution Inflammatory Syndrome (TB-IRIS).

  • Treatment Principles:

High‑Yield Points - ⚡ Biggest Takeaways

  • HIV accelerates HBV and HCV progression to cirrhosis and liver cancer. Screen all new HIV patients for these co-infections.
  • Tenofovir-based ART is dual-acting and preferred for HIV/HBV co-infection.
  • Screen for latent TB in all HIV patients; a tuberculin skin test (TST) ≥5 mm is considered positive.
  • Starting ART can trigger Immune Reconstitution Inflammatory Syndrome (IRIS), paradoxically worsening TB symptoms.
  • Watch for drug-drug interactions between HCV direct-acting antivirals (DAAs) and antiretroviral therapy.

Practice Questions: HIV co-infections (HBV, HCV, TB)

Test your understanding with these related questions

A scientist is researching the long term effects of the hepatitis viruses on hepatic tissue. She finds that certain strains are oncogenic and increase the risk of hepatocellular carcinoma. However, they appear to do so via different mechanisms. Which of the following answer choices correctly pairs the hepatitis virus with the correct oncogenic process?

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Flashcards: HIV co-infections (HBV, HCV, TB)

1/10

_____ is the matrix protein of HIV

TAP TO REVEAL ANSWER

_____ is the matrix protein of HIV

p17

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