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HIV Tat causes synapse loss in a mouse model of HIV-associated neurocognitive disorder that is independent of the

Jennetta W Hammond1, Wen Q Qiu1, Daniel F Marker1

  • 1Center for Neurotherapeutics Discovery, University of Rochester Medical Center, Rochester, New York.

Glia
|October 17, 2018
PubMed

Insights

The complement system, specifically C1q, does not drive synapse loss in a mouse model of HIV-associated neurocognitive disorders (HAND). This finding challenges the role of the classical complement cascade in Tat-induced neuroinflammation and synaptic pruning.

Area of Science:

  • Neuroscience
  • Immunology
  • Virology

Background:

  • HIV-associated neurocognitive disorders (HAND) involve microglial activation, inflammation, and synaptic loss, persisting even with combination antiretroviral therapy (cART).
  • HIV Tat protein contributes to neurotoxicity, synapse elimination, and persistent neuroinflammation, independent of viral replication.
  • Complement-mediated synapse elimination is a known mechanism in development and disease, prompting investigation into its role in HAND.

Purpose of the Study:

  • To investigate whether the complement system is required for synapse loss in a mouse model of HAND induced by cortical Tat injection.
  • To determine if the early complement pathway components C1q and C3 are involved in Tat-induced synaptic pruning.

Main Methods:

  • Cortical Tat injection in wild-type (WT) and C1qa knockout (KO) mice.
  • Assessment of synapse density, microgliosis, and complement component levels (C1q, C3) at 7 and 28 days post-injection.

Main Results:

  • Tat injection led to elevated C1q and C3 levels, microgliosis, and significant synapse loss in WT mice.
  • C1qa knockout mice exhibited comparable levels of Tat-induced synapse loss to WT mice.
  • The C1q-initiated classical complement cascade was not the driving mechanism for synapse removal in this HAND model.

Conclusions:

  • The classical complement cascade, initiated by C1q, is not essential for Tat-induced synapse loss in the studied mouse model.
  • These findings suggest alternative pathways mediate synapse elimination during HIV Tat-induced neuroinflammation.
  • Further research is needed to elucidate the precise mechanisms of synapse loss in HAND.
Keywords:
C1qHIVTatcomplementsynapse

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