TY - JOUR
T1 - Establishment of latent herpes simplex virus type 1 infection in resistant, sensitive, and immunodeficient mouse strains
AU - Ellison, Aaron R.
AU - Yang, Li
AU - Voytek, Cynthia
AU - Margolis, Todd P.
N1 - Funding Information:
We thank Alma Pagliarula for technical assistance and Anita Edge-combe for help in preparation of the manuscript. This work was supported by National Institutes of Health Grants NIH10008 and NIH02162 and a Research to Prevent Blindness Lew Wasswerman Merit Award (T.P.M.)
PY - 2000/3/1
Y1 - 2000/3/1
N2 - Productive infection with herpes simplex virus (HSV) type 1 is limited by both innate and adaptive immune mechanisms. The purpose of the current study was to determine whether these mechanisms also play a role in the establishment of latent HSV infection. First we examined the trigeminal ganglia (TG) of severe combined immunodeficiency (SOLD), interferon-γ knockout (GKO), and beige (a strain deficient in natural killer cell activity) mice following ocular inoculation with HSV. Although infection of SCID mice was invariably lethal, we consistently found latently infected neurons in the TG of these animals at 2-4 days postinoculation. HSV infection of GKO and beige mice, while not lethal, was characterized by a greater number of productively infected TG neurons and/or a delay in the time to peak productive infection compared to C57BL/6 controls. However, as assayed by both in situ hybridization for LAT expression and quantitative PCR (Q-PCR) for viral DNA, we found that HSV established a latent infection in GKO and beige mice as efficiently as in C57BL/6 controls. We subsequently examined the TG of 'HSV-sensitive' strains of mice (Swiss-Webster, CBA, and BALB/c) following ocular infection with HSV. At the peak of acute ganglionic infection the number of productively infected TG neurons in each of these mouse strains was about sevenfold greater than in the 'HSV-resistant' strain C57BL/6, consistent with previously reported differences in susceptibility to lethal challenge with HSV. However, as assayed by both in situ hybridization for LAT and Q-PCR for viral DNA, we found that HSV established a latent infection in Swiss-Webster, CBA, and BALB/c mice as efficiently as in C57BL/6 controls. We conclude that HSV efficiently establishes latent infection in the TG of mice in the absence of innate and adaptive immune mechanisms that Ere essential for limiting productive viral infection. (C) 2000 Academic Press.
AB - Productive infection with herpes simplex virus (HSV) type 1 is limited by both innate and adaptive immune mechanisms. The purpose of the current study was to determine whether these mechanisms also play a role in the establishment of latent HSV infection. First we examined the trigeminal ganglia (TG) of severe combined immunodeficiency (SOLD), interferon-γ knockout (GKO), and beige (a strain deficient in natural killer cell activity) mice following ocular inoculation with HSV. Although infection of SCID mice was invariably lethal, we consistently found latently infected neurons in the TG of these animals at 2-4 days postinoculation. HSV infection of GKO and beige mice, while not lethal, was characterized by a greater number of productively infected TG neurons and/or a delay in the time to peak productive infection compared to C57BL/6 controls. However, as assayed by both in situ hybridization for LAT expression and quantitative PCR (Q-PCR) for viral DNA, we found that HSV established a latent infection in GKO and beige mice as efficiently as in C57BL/6 controls. We subsequently examined the TG of 'HSV-sensitive' strains of mice (Swiss-Webster, CBA, and BALB/c) following ocular infection with HSV. At the peak of acute ganglionic infection the number of productively infected TG neurons in each of these mouse strains was about sevenfold greater than in the 'HSV-resistant' strain C57BL/6, consistent with previously reported differences in susceptibility to lethal challenge with HSV. However, as assayed by both in situ hybridization for LAT and Q-PCR for viral DNA, we found that HSV established a latent infection in Swiss-Webster, CBA, and BALB/c mice as efficiently as in C57BL/6 controls. We conclude that HSV efficiently establishes latent infection in the TG of mice in the absence of innate and adaptive immune mechanisms that Ere essential for limiting productive viral infection. (C) 2000 Academic Press.
UR - http://www.scopus.com/inward/record.url?scp=0034007315&partnerID=8YFLogxK
U2 - 10.1006/viro.1999.0158
DO - 10.1006/viro.1999.0158
M3 - Article
C2 - 10683323
AN - SCOPUS:0034007315
SN - 0042-6822
VL - 268
SP - 17
EP - 28
JO - Virology
JF - Virology
IS - 1
ER -