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Oligodendrocytes from human donors differ in resistance to herpes simplex virus 1 (HSV‐1)
Author(s) -
Kastrukoff Lorne F.,
Kim Seung U.
Publication year - 2002
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.10043
Subject(s) - biology , herpes simplex virus , virology , hol , virus , viral replication , in vitro , cell culture , herpesviridae , immunology , viral disease , genetics , computer science , programming language
Primary cultures of human oligodendrocytes (HOLs) were established from six different donors. Differences in resistance to infection with herpes simplex virus 1 (HSV‐1) were determined between the primary cultures of HOL in tissue culture infective dose 50 (TCID 50 ), indirect immunofluoresence (IF), and serial electron microscopy (EM) studies. Virus production at different multiplicities of infection (MOIs) indicated that differences in HSV‐1 replication were statistically significant and MOI‐dependent. Overall, virus yield from the HOL cultures infected at an MOI of 1 increased up to 6 days postinfection (PI); no additional enhancement occurred at 7 days PI. However, differences in the replication capacity of the six HOL cultures observed at 5 days PI persisted at 6 and 7 days PI. When taken together, the results of these investigations indicate that, similar to experimental animals, resistance to HSV‐1 differs between primary cultures of HOL and is donor‐dependent. The results also raise the possibility that similar to experimental animals, resistance to HSV‐1, mediated at the level of HOL, may be genetically determined. Furthermore, permissive infections of primary cultures of HOL were established with HSV‐1 over a wide range of MOIs, similar to results obtained with viral infection of primary murine oligodendrocytes, but neither latent nor abortive infections of HOL were induced in vitro, even at very low MOIs. Resistance to HSV‐1, mediated by glial cells, is a nonimmune mechanism that may influence the development of acute CNS infection in man as well as individual susceptibility to this virus. GLIA 38:87–92, 2002. © 2002 Wiley‐Liss, Inc.