Human Immunodeficiency Virus (HIV)

 

Acquired Immunodeficiency Syndrome (AIDS)

etiology:

strains: HIV-1 and HIV-2

a retrovirus: virus that contain two single-strand linear RNA molecules per virion and reverse transcriptase (RNA to DNA)

  • T helper cells, C4 cells targeted
  • immunosuppression occurs
  • chronic progressive condition

 

clinically discovered early 1980-1981

isolated and first research paper published 1983

  • incubation periods ranges from 1-3 months, may be as long as ten years

 

Manifestations:

  • development of opportunistic infections and cancers
  • full blown AIDS – C4 cells <200ul

 

transmission

  • contaminated blood
  • contaminated tissue
  • contaminated bodily fluids
  • sexual transmission
  • maternal-fetal transmission across placenta
  • infant transmission from mother at delivery and through lactation
  • 0.3% risk to health care workers with proper technique – needle stick injury
  • needle stick injuries – infection depends on site, depth and viral load of sample

 

Pathophysiology 3 phases:

  • infection characterized by high viral load & decreased CD4 count (assay for CD4 cell-surface receptors)
  • Thelper cells and viral load are inversely related
  • virus targets specific cell surface receptor – that of CD4
  • resulting in HIV destruction of T helper cells

 

Primary phase

  • infection establishment in weeks to months
  • viral antibody detection – seroconversion
  • 10 days for normal viral infection Ab production peak – with HIV, 3 months post initial contact
  • window period – no conclusive results until Ab lvls reach ELISA or Western blot detection sensitivity

Latent period

  • may be asymptomatic for years
  • T helper cell destruction occurs at a variable rate (affecting individuals at different rates)
  • recurrent respiratory infections occur as Thelper cell levels decline (not yet a critical levels)
  • chronic fatigue – energy routed to immune defenses

 

Full blown AIDS

  • CD4 cells below 200ul
  • 60-70% of infected individuals convert to AIDS within 10yrs of infection
  • others immune cells (macrophages, B cells) possessing CD4 cell-surface receptors are also targeted

 

AIDS characteristic manifestations

  1. increase in new opportunistic infections
  2. reactivation of latent viral infections eg. HepB, herpetics etc

 

  • primary infection is the HIV
  • secondary infections are latent and opportunistic infections

 

Dx

lab tests”

  1. ELISA – enzyme linked immunosorbent assay
  • used to detect HIV Ab levels
  • must be run after 3 mo window period (whole virus serves as the Ag) for Ab levels to be sufficient for detection
  • antivirals started at time of potential contamination, tested at time of infection, then at 3mo
     
  1. Western Blot assay
  • a test to identify and locate proteins. Can be used to detect antibodies in serum
  • a complex mixture of size-separated proteins is fixed to a solid support, and then probed with a labelled antibody
  • (measures specific Ag on viral particle, therefore more specific that ELISA)
     
  1. PCR – polymerase chain rxn
  • measures virus itself – may be done on day 1 of potential infection
  • Method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide.
     

Manifestations: clinical presentation

  • varies on disease stage and secondary infections present
  • typical secondary infections:

Respiratory:

  • TB
  • pneumonia

 

GI infections

  • gastroenteritis
  • GI bleeds

Nervous System infection damage results in

  • dementia
  • encephalopathy

Cancers

  • kaposi’s sarcoma (endothelial cells – that line blood vessels)
  • non-hodgkin’s lymphoma
  • cervical cancer

 

Management:

  • antiviral drug cocktail to reduce chance of resistance
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