Point mutations in herpes simplex virus type 1 oriL, but not in oriS, reduce pathogenesis during acute infection of mice and impair reactivation from latency

Journal of Virology

Volumn 80, Issue 1, 2006, Pages 440-450

  Balliet, John W ^a   Schaffer, Priscilla A ^a  

^a BETH ISRAEL DEACONESS MEDICAL CENTER   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; CELL CULTURE; CONTROLLED STUDY; DNA REPLICATION; DNA SYNTHESIS; HERPES SIMPLEX VIRUS 1; HERPES VIRUS; LIFE CYCLE; MALE; MOUSE; NONHUMAN; PATHOGENESIS; POINT MUTATION; PRIORITY JOURNAL; RHOMBENCEPHALON; TRIGEMINUS GANGLION; VIRUS LATENCY; VIRUS MUTANT; VIRUS REACTIVATION;

ANIMALS; CERCOPITHECUS AETHIOPS; DNA REPLICATION; DNA, VIRAL; HERPES SIMPLEX; HERPESVIRUS 1, HUMAN; HUMANS; MICE; MICE, INBRED ICR; POINT MUTATION; REPLICATION ORIGIN; VERO CELLS; VIRUS ACTIVATION; VIRUS LATENCY;

ANIMALIA; DORIS; HERPESVIRIDAE; HUMAN HERPESVIRUS 1;

EID: 33645957647     PISSN: 0022538X     EISSN: None     Source Type: Journal    
DOI: 10.1128/JVI.80.1.440-450.2006     Document Type: Article

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