Recombinant Cell Lines Expressing shRNA Targeting Herpes Simplex Virus 2 VP16 Inhibit Virus Replication

Intervirology ◽  
2012 ◽  
Vol 55 (6) ◽  
pp. 426-434 ◽  
Author(s):  
Rui Zhang ◽  
Yan Wang ◽  
Bo Song ◽  
Zhi Qiang Han ◽  
Yu Ming Xu
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Cell Lines ◽  
Virus Replication ◽  
Inhibit Virus Replication ◽  
Recombinant Cell ◽  
Simplex Virus ◽  
Herpes Simplex Virus 2

Further Characterization of the Potent and Prolonged Inhibition of Herpes Simplex Virus Replication in Human Cell Lines by Penciclovir

1996 ◽  
Vol 7 (3) ◽  
pp. 128-137 ◽  
Author(s):  
T.H. Bacon ◽  
B.A. Howard
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Cell Lines ◽  
Virus Replication ◽  
Human Cell ◽  
Human Cell Lines ◽  
Potent Inhibition ◽  
Multiple Cycles ◽  
Simplex Virus ◽  
Hsv 1

The replication of herpes simplex virus type 1 (HSV-1) or HSV-2 in MRC-5 cells infected at 0.01 pfu cell−1 treated continuously for 72 h, was inhibited more efficiently by penciclovir than aciclovir ( p = 0.0001). However, multiple cycles of replication were required in order to distinguish the compounds. Virus from cultures treated for 72 h with either compound, at 3 or 10 μg ml−1 was resistant to penciclovir and aciclovir (50% effective concentrations > 10 μg ml−1), but infectivity titres of supernatants from these aciclovirtreated cultures were higher than for penciclovir. Increased production of resistant virus in aciclovirtreated cultures may be the consequence of the less potent inhibition of virus replication by aciclovir. Penciclovir caused prolonged inhibition of HSV-1 and HSV-2 replication in three human cell lines infected at 1 pfu cell−1 following treatment for 18 h, whereas virus replication resumed rapidly after withdrawal of aciclovir. Neither compound showed prolonged activity after 18 h treatment, when the multiplicity of infection was reduced to 0.01 pfu cell−1. This surprising observation prompted experiments testing the effect of repeated pulse treatment in cultures infected at low multiplicity. Penciclovir inhibited HSV-1 replication significantly more effectively than aciclovir in MRC-5 cells infected at 10−4 pfu cell−1 treated daily for 6 h ( p < 0.001, n = 5) but only a trend was observed for HSV-2 ( p = 0.06, n = 6).

scholarly journals Herpes Simplex Virus ICP0 and ICP34.5 Counteract Distinct Interferon-Induced Barriers to Virus Replication

2002 ◽  
Vol 76 (4) ◽  
pp. 1995-1998 ◽  
Author(s):  
Karen L. Mossman ◽  
James R. Smiley
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Cell Lines ◽  
Virus Replication ◽  
Vero Cells ◽  
Differentially Expressed ◽  
Viral Transcription ◽  
Established Cell Lines ◽  
Established Cell ◽  
Simplex Virus

ABSTRACT Interferon inhibits virus replication through multiple mechanisms. Here we show that herpes simplex virus proteins ICP0 and ICP34.5 overcome interferon-induced barriers to viral transcription and translation, respectively. These cytokine-induced antiviral mechanisms are differentially expressed in established cell lines: U2OS cells do not mount the IFN-induced mechanism targeted by ICP0, and Vero cells may be defective for the mechanism targeted by ICP34.5.

scholarly journals A Herpes Simplex Virus 2 (HSV-2) gD Mutant Impaired for Neural Tropism Is Superior to an HSV-2 gD Subunit Vaccine To Protect Animals from Challenge with HSV-2

2015 ◽  
Vol 90 (1) ◽  
pp. 562-574 ◽  
Author(s):  
Kening Wang ◽  
Kyle N. Goodman ◽  
Daniel Y. Li ◽  
Mark Raffeld ◽  
Mayra Chavez ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Genital Herpes ◽  
Virus Replication ◽  
Dorsal Root ◽  
Subunit Vaccine ◽  
Challenge Virus ◽  
A Subunit ◽  
Simplex Virus ◽  
Herpes Simplex Virus 2

ABSTRACTA recent phase 3 trial with soluble herpes simplex virus 2 (HSV-2) glycoprotein D (gD2t) in adjuvant failed to show protection against genital herpes. We postulated that live attenuated HSV-2 would provide more HSV antigens for induction of virus-specific antibodies and cellular immunity than would gD2t. We previously reported an HSV-2 mutant, HSV2-gD27, in which the nectin-1 binding domain of gD2 is altered so that the virus is impaired for infecting neural cells, but not epithelial cells,in vitroand is impaired for infecting dorsal root ganglia in mice (K. Wang, J. D. Kappel, C. Canders, W. F. Davila, D. Sayre, M. Chavez, L. Pesnicak, and J. I. Cohen, J Virol 86:12891–12902, 2012, doi:10.1128/JVI.01055-12). Here we report that the mutations in HSV2-gD27 were stable when the virus was passaged in cell culture and during acute infection of mice. HSV2-gD27 was attenuated in mice when it was inoculated onto the cornea, intramuscularly (i.m.), intravaginally, and intracranially. Vaccination of mice i.m. with HSV2-gD27 provided better inhibition of challenge virus replication in the vagina than when the virus was used to vaccinate mice intranasally or subcutaneously. Comparison of i.m. vaccinations with HSV2-gD27 versus gD2t in adjuvant showed that HSV2-gD27 induced larger reductions of challenge virus replication in the vagina and reduced latent viral loads in dorsal root ganglia but induced lower serum neutralizing antibody titers than those obtained with gD2t in adjuvant. Taken together, our data indicate that a live attenuated HSV-2 vaccine impaired for infection of neurons provides better protection from vaginal challenge with HSV-2 than that obtained with a subunit vaccine, despite inducing lower titers of HSV-2 neutralizing antibodies in the serum.IMPORTANCEGenital herpes simplex is one of the most prevalent sexually transmitted diseases. Though HSV-2 disease is usually mild, it can be life threatening in neonates and immunocompromised persons. In addition, genital herpes increases the frequency of HIV infection and transmission. HSV-2 maintains a latent infection in sensory neurons and cannot be cleared with antiviral drugs. The virus frequently reactivates, resulting in virus shedding in the genital area, which serves as a source for transmission. A prophylactic vaccine is needed to prevent disease and to control the spread of the virus. Previous human trials of subunit vaccines have been unsuccessful. Here we report the results of vaccinating mice with a new type of live attenuated HSV-2 vaccine that is impaired for infection of neurons and provides better protection of mice than that obtained with a subunit vaccine. The strategy of altering the cell tropism of a virus is a new approach for a live attenuated vaccine.

Corrigendum to “Cetylpyridinium chloride blocks herpes simplex virus replication in gingival fibroblasts” [Anti. Res. 179 (2020) 104818]

2021 ◽  
Vol 188 ◽  
pp. 105022
Author(s):  
Diana M. Alvarez ◽  
Luisa F. Duarte ◽  
Nicolas Corrales ◽  
Patricio C. Smith ◽  
Pablo A. González
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Virus Replication ◽  
Cetylpyridinium Chloride ◽  
Gingival Fibroblasts ◽  
Simplex Virus

scholarly journals Disseminated Herpes Simplex Virus 2 as a Complication of Pregnancy

IDCases ◽  
2021 ◽  
pp. e01107
Author(s):  
Lauren Bougioukas ◽  
Rachel B.C. Psoinos ◽  
David C. Jones ◽  
Erin A. Morris ◽  
Andrew J. Hale
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Simplex Virus ◽  
Herpes Simplex Virus 2

scholarly journals Control of Herpes Simplex Virus Replication Is Mediated through an Interferon Regulatory Factor 3-Dependent Pathway

2009 ◽  
Vol 83 (23) ◽  
pp. 12399-12406 ◽  
Author(s):  
Vineet D. Menachery ◽  
David A. Leib
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Virus Replication ◽  
Early Recognition ◽  
Critical Role ◽  
Type I ◽  
Type I Ifn ◽  
Regulatory Factor ◽  
Simplex Virus ◽  
Hsv 1

ABSTRACT The type I interferon (IFN) cascade is critical in controlling viral replication and pathogenesis. Recognition pathways triggered by viral infection rapidly induce the type I IFN cascade, often in an IFN regulatory factor 3 (IRF-3)-dependent fashion. This dependence predicts that loss of IRF-3 would render early recognition pathways inoperative and thereby impact virus replication, but this has not been observed previously with herpes simplex virus type 1 (HSV-1) in vitro. In this study, HSV-1-infected IRF-3−/− bone marrow-derived dendritic cells (BMDCs) and macrophages supported increased HSV replication compared to control cells. In addition, IRF-3-deficient BMDCs exhibited delayed type I IFN synthesis compared to control cells. However, while IFN pretreatment of IRF-3−/− BMDCs resulted in reduced virus titers, a far greater reduction was seen after IFN treatment of wild-type cells. This suggests that even in the presence of exogenously supplied IFN, IRF-3−/− BMDCs are inherently defective in the control of HSV-1 replication. Together, these results demonstrate a critical role for IRF-3-mediated pathways in controlling HSV-1 replication in cells of the murine immune system.

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