Journal
JOURNAL OF VIROLOGY
Volume 80, Issue 17, Pages 8664-8675Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.00498-06
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Funding
- NEI NIH HHS [R01 EY013867, EY 13867] Funding Source: Medline
- NIAID NIH HHS [AI 52341, R29 AI038873, R01 AI052341, R01 AI038873, R21 AI038873, AI 38873] Funding Source: Medline
- NIGMS NIH HHS [R01 GM 50740, F32 GM067519, R01 GM050740, R56 GM050740] Funding Source: Medline
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Herpes simplex virus type 1 (HSV-1) virions, like those of all herpesviruses, contain a proteinaceous layer termed the tegument that lies between the nucleocapsid and viral envelope. The HSV-1 tegument is composed of at least 20 different viral proteins of various stoichiometries. VP22, the product of the U(L)49 gene, is one of the most abundant tegument proteins and is conserved among the alphaherpesviruses. Although a number of interesting biological properties have been attributed to VP22, its role in HSV-1 infection is not well understood. In the present study we have generated both a U(L)49-null virus and its genetic repair and characterized their growth in both cultured cells and the mouse cornea. While single-step growth analyses indicated that VP22 is dispensable for virus replication at high multiplicities of infection (MOIs), analyses of plaque morphology and intra- and extracellular multistep growth identified a role for VP22 in viral spread during HSV-1 infection at low MOIs. Specifically, VP22 was not required for either virion infectivity or cell-cell spread but was required for accumulation of extracellular virus to wild-type levels. We found that the absence of VP22 also affected virion composition. Intracellular virions generated by the U(L)49-null virus contained reduced amounts of ICPO and glycoproteins E and D compared to those generated by the wild-type and U(L)49-repaired viruses. In addition, viral spread in the mouse cornea was significantly reduced upon infection with the U(L)49-null virus compared to infection with the wild-type and U(L)49-repaired viruses, identifying a role for VP22 in viral spread in vivo as well as in vitro.
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