Viral genetics modulate orolabial HSV-1 shedding in humans.
Ramchandani MS, Jing L, Russell RM, Tran T, Laing KJ, Magaret AS, Selke S, Cheng A, Huang ML, Xie H, Strachan E, Greninger AL, Roychoudhury P, Jerome KR, Wald A, Koelle DM.
Orolabial herpes simplex virus type 1 (HSV-1) infection has wide severity spectrum in immunocompetent persons. To study the role of viral genotype and host immunity, we characterized oral HSV-1 shedding rates, host cellular response and genotyped viral strains in mono- (MZ) and dizygotic (DZ) twins.
29 MZ and 22 DZ HSV-1 seropositive twin pairs were evaluated for oral HSV-1 shedding for 60 days. HSV-1 strains from twins were genotyped as identical or different. CD4 T-cell responses to HSV-1 proteins were studied.
The median oral HSV shedding rate was 9% (mean 10.2%). A positive correlation between shedding rates within all twin pairs was observed, and in MZ and DZ twins. In twins with sufficient HSV-1 DNA to genotype, 15 had the same and 14 had different strains. Viral shedding rates were correlated for those with the same but not different strains. The median number of HSV-1 ORFs recognized per person was 16. The CD4 T-cell response agreement to different HSV-1 ORFs was greater between MZ twins, than between unrelated persons (p=0.002).
Viral strain characteristics likely contribute to oral HSV-1 shedding rates.
Viral genetics modulate orolabial HSV-1 shedding in humans. J Infect Dis. 2019 Mar 15;219(7):1058-1066.