NAVLE Primates

Simian Immunodeficiency Virus (SIV) and Simian AIDS – NAVLE Study Guide

Simian immunodeficiency virus (SIV) is a lentivirus belonging to the family Retroviridae that naturally infects over 45 species of nonhuman primates.

Overview and Clinical Importance

Simian immunodeficiency virus (SIV) is a lentivirus belonging to the family Retroviridae that naturally infects over 45 species of nonhuman primates. While SIV is typically non-pathogenic in its natural African primate hosts due to coevolution, cross-species transmission to non-natural hosts, particularly Asian macaques, results in a severe immunodeficiency syndrome known as simian AIDS (SAIDS). This disease closely parallels human AIDS and serves as the primary animal model for HIV research. For NAVLE preparation, understanding SIV is essential for questions on primate medicine, comparative immunology, and zoonotic disease potential.

SIV Strain Natural Host Clinical Significance
SIVsmm Sooty mangabeys Non-pathogenic in natural host; precursor to HIV-2; causes SAIDS in macaques
SIVcpz Chimpanzees Can cause AIDS-like disease in chimps; precursor to HIV-1
SIVagm African green monkeys Non-pathogenic despite high viral loads; seroprevalence 60-70% in wild populations
SIVmac Rhesus macaques (captive) Not found in wild Asian macaques; experimental strain causing rapid disease progression

Etiology and Viral Classification

Viral Structure and Genome

SIV is a single-stranded, positive-sense RNA virus measuring approximately 80-100 nanometers in diameter. Like all lentiviruses, SIV possesses:

  • Lipid envelope derived from host cell membrane containing viral glycoproteins gp120 and gp41
  • Matrix protein (MA/p17) beneath the envelope
  • Conical capsid (CA/p24) containing two copies of viral RNA and reverse transcriptase
  • Nucleocapsid proteins (NC) complexed with viral genomic RNA

The SIV genome contains standard retroviral genes (gag, pol, env) plus accessory genes (tat, rev, nef, vif, vpr). The reverse transcriptase enzyme enables conversion of viral RNA to DNA, which integrates into the host genome–a hallmark of lentivirus pathogenesis.

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