Open AccessReactivation of herpes simplex virus type 2 from a quiescent state by human cytomegalovirus.
Author(s) -
Anamaris M. Colberg-Poley,
Harriet C. Isom,
Fred Rapp
Publication year - 1979
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.76.11.5948
Subject(s) - herpes simplex virus , superinfection , virology , biology , cytomegalovirus , human cytomegalovirus , herpesviridae , virus , simplexvirus , immune system , viral replication , virus quantification , immunology , viral disease
The ability of human cytomegalovirus to stimulate replication of herpes simplex virus type 2 (HSV-2) was examined. The system used involved HSV-2-infected human embryonic lung cells under conditions (39.5-40 degrees C) in which HSV-2 remains undetectable. Reactivation of HSV-2 was maximal and persisted for the longest duration when cultures were superinfected with 0.02 plaque-forming unit of human cytomegalovirus per cell. Infectious HSV-2 appeared 2 days after superinfection with human cytomegalovirus and ranged from 10(2) to 10(6) plaque-forming units per culture. Virus reactivated from these cultures was neutralized by rabbit immune serum produced against HSV-2. The specificity of this interaction was demonstrated by various criteria: production of HSV-2 was not observed in cultures treated with mock infecting fluid, and inactivation of human cytomegalovirus by heat, ultraviolet irradiation, or immune serum prior to superinfection eliminated its ability to induce HSV-2 replication. These results sugges that interaction between these two human herpesviruses may be of importance in herpesvirus latency in vivo.