Loss of inducible virus in CD45RA naive cells after human immunodeficiency virus-1 entry accounts for preferential viral replication in CD45RO memory cells.

Important note: Information in this article was accurate in 1997. The state of the art may have changed since the publication date.

Loss of inducible virus in CD45RA naive cells after human immunodeficiency virus-1 entry accounts for preferential viral replication in CD45RO memory cells.

Blood. 1997 Mar 1;89(5):1635-41. Unique Identifier : AIDSLINE MED/97210573
Woods TC; Roberts BD; Butera ST; Folks TM; Retrovirus Diseases Branch, Centers for Disease Control and; Prevention, Atlanta, GA 30333, USA.

Abstract: Controversy exists concerning the preferential infection and replication of human immunodeficiency virus-1 (HIV-1) within naive (CD45RA+) and memory (CD45RO+) subsets of CD4+ lymphocytes. To explore the susceptibility of these subsets to HIV-1 infection, we purified CD45RA+/CD4+ (RA) and CD45RO+/CD4+ (RO) cells from normal donors and subjected them to a novel monokine activation culture scheme. Following HIV-1 infection and interleukin-2 (IL-2) induction, viral production measured on day 13 was 19-fold greater in RO cultures compared with RA cultures. IL-2-stimulated proliferation in uninfected control cultures was equivalent. To explore the mechanisms by which RA cells were reduced in viral production capacity, RA and RO cells were exposed to HIV-1 followed by treatment with trypsin, and then phytohemagglutinin antigen (PHA)-stimulated at days 4, 7, and 10 postinfection. HIV-1 production in day 4 postinfection RA and RO cultures was analogous, indicating that viral fusion and entry had occurred in both cell types. However, whereas similarly treated day 7 and 10 postinfection RO cultures produced virus, HIV-1 was markedly reduced or lost in the corresponding RA cultures. These results suggest that a temporally labile postfusion HIV-1 complex exists in unstimulated RA cells that requires cellular activation signals beyond that provided by IL-2 alone for productive infection.

Keywords: *Antigens, CD45/IMMUNOLOGY *CD4-Positive T-Lymphocytes/VIROLOGY *HIV Infections *HIV-1/PHYSIOLOGY *T-Lymphocyte Subsets/VIROLOGY *Virus Replication/IMMUNOLOGY
970630
M9761222

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