Efficient synthesis of viral nucleic acids following monocyte infection by HIV-1

Nina Heinzinger, Lisa Baca-Regen, Mario Stevenson, Howard Eliot Gendelman

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

The replication of human immunodeficiency virus type 1 in mononuclear phagocytes (blood monocytes, tissue macrophages, and dendritic cells) is an important feature of HIV-1 pathogenesis. Although most primary HIV-1 isolates are able to productively infect monocytes, some reports suggest that rates of viral DNA synthesis and virus replication are reduced in HIV-1-infected monocytes as compared to infected T cells. In this study we compare kinetics of viral DNA synthesis in CD4+ T cells and monocytes following HIV-1 infection. Our results indicate that reverse transcription of viral nucleic acids following infection of monocytes occurs at rates equal to or greater than that observed following infection of T cells. These studies reveal no postentry restrictions to HIV-1 replication following infection in monocytes. Moreover, the results support the notion that both monocytes and CD4+ T cells are equally permissive for virus replication in infected individuals.

Original languageEnglish (US)
Article number95800972
Pages (from-to)731-735
Number of pages5
JournalVirology
Volume206
Issue number1
DOIs
StatePublished - Jan 1 1995

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Nucleic Acids
HIV-1
Monocytes
Infection
T-Lymphocytes
Viral DNA
Virus Replication
DNA Viruses
Phagocytes
DNA Replication
Dendritic Cells
Reverse Transcription
HIV Infections
Macrophages

ASJC Scopus subject areas

  • Virology

Cite this

Efficient synthesis of viral nucleic acids following monocyte infection by HIV-1. / Heinzinger, Nina; Baca-Regen, Lisa; Stevenson, Mario; Gendelman, Howard Eliot.

In: Virology, Vol. 206, No. 1, 95800972, 01.01.1995, p. 731-735.

Research output: Contribution to journalArticle

Heinzinger, Nina ; Baca-Regen, Lisa ; Stevenson, Mario ; Gendelman, Howard Eliot. / Efficient synthesis of viral nucleic acids following monocyte infection by HIV-1. In: Virology. 1995 ; Vol. 206, No. 1. pp. 731-735.
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