
Short Communication: The Dead Cell: A Potent Escort for HIV Type 1 Transinfection
Author(s) -
Robert E. Sealy,
Bart G. Jones,
Sherri L. Surman,
Julia L. Hurwitz
Publication year - 2009
Publication title -
aids research and human retroviruses
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.993
H-Index - 92
eISSN - 1931-8405
pISSN - 0889-2229
DOI - 10.1089/aid.2009.0021
Subject(s) - cell , internalization , biology , endocytosis , cell fusion , antibody , in vitro , virology , microbiology and biotechnology , cell type , cell culture , virus , immunology , genetics
HIV-1 transinfection is a process by which one cell acts as an HIV-1 "escort" to enhance infection of another. There has recently been much debate concerning (1) the types of cells that may act as escorts, (2) requirements for virus internalization by the escort, and (3) the sensitivity of transinfection to inhibition by neutralizing antibodies. To address these questions, transinfection was monitored by incubating target cells with HIV-1 in the presence or absence of mouse or human cells as candidate escorts in vitro. After a 2-day culture, target cells were tested for levels of HIV-1 infection. Results showed that a variety of murine and human cells were capable escorts for HIV-1 transinfection. Cell integrity was not required, as escorts could be freeze/thawed (or fractionated to yield purified membranes/microsomes) prior to their incubation with HIV-1. In fact, the freeze/thawed or fractionated cells were often superior to their viable counterparts as mediators of transinfection. The process was sensitive to antibody neutralization. Confirmatory experiments were conducted with more than one target cell and more than one source of HIV-1. Results demonstrated that there may be multiple cell types and mechanisms with which transinfection can be accomplished. Apparently the simple binding of fragmented escort membranes to HIV-1 may be sufficient to enhance virus fusion or endocytosis at the target cell surface. The fact that dead cells or membranes can support this activity may explain, at least in part, the high frequency of human HIV-1 infections at sites of tissue damage.