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Maintenance of Human Immunodeficiency Virus Type‐1 Proviral DNA in Human Fetal Dorsal Root Ganglia Neural Cells Following a Nonproductive Infection
Journal article   Open access   Peer reviewed

Maintenance of Human Immunodeficiency Virus Type‐1 Proviral DNA in Human Fetal Dorsal Root Ganglia Neural Cells Following a Nonproductive Infection

Charles Kunsch and Brian Wigdahl
Journal of leukocyte biology, v 49(5), pp 505-510
May 1991
PMID: 2016571
url
https://doi.org/10.1002/jlb.49.5.505View
Published, Version of Record (VoR)Maybe Open Access (Publisher Bronze) Open

Abstract

HIV‐1 gag antigen glial cells nervous system
Infection of the nervous system by human immunodeficiency virus type‐1 (HIV‐1) has been implicated in the generation of acquired immunodeficiency syndrome (AIDS)‐associated neurologic dysfunction and direct infection of glia has been suggested as one of the potential mechanisms leading to deterioration of nervous system function. We have been examining the interaction of HIV‐1 with the developing peripheral nervous system in vitro, and have previously shown that HIV‐1 infection of primary human fetal dorsal root ganglia (DRG) neural cells resulted in HIV‐1 gag antigen expression in approximately 70% of the glial cell subpopulation with little, if any, cytopathic damage to the infected cells. Accumulation of HIV‐1 gag antigens and viral mRNA reached a maximum by 2–3 days postinfection and declined thereafter to minimally detectable levels in the surviving neural cell population. In addition, infection of the fetal DRG neural cells appeared to be abortive or nonproductive, with little if any, infectious progeny virus production. However, we have been able to detect HIV‐1‐specific proviral DNA as late as 24 days postinfection by polymerase chain reaction amplification and subsequent DNA blot hybridization. These results suggest that accumulation of HIV‐1 structural proteins without the assembly and release of mature virus in HIV‐1‐infected human fetal DRG neural cells results in a nonproductive infection and maintenance of HIV‐1 proviral DNA in the infected cell population.

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Web of Science research areas
Cell Biology
Hematology
Immunology
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