scholarly journals Analysis of herpes simplex virus 1 and 2 infection in women with high risk sexual behaviour in Mexico

1999 ◽  
Vol 28 (3) ◽  
pp. 571-576 ◽  
Author(s):  
C. J. Conde-Glez ◽  
L. Juarez-Figueroa ◽  
F. Uribe-Salas ◽  
P. Hernandez-Nevarez ◽  
D. S. Schmid ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
High Risk ◽  
Sexual Behaviour ◽  
Herpes Simplex Virus 1 ◽  
High Risk Sexual Behaviour ◽  
Risk Sexual Behaviour ◽  
Simplex Virus

scholarly journals HIV and herpes simplex virus type 2 epidemiological synergy: misguided observational evidence? A modelling study

2017 ◽  
Vol 94 (5) ◽  
pp. 372-376 ◽  
Author(s):  
Ryosuke Omori ◽  
Nico Nagelkerke ◽  
Laith J Abu-Raddad
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
High Risk ◽  
Sexual Behaviour ◽  
Observational Studies ◽  
Biological Interaction ◽  
The Mean ◽  
Hiv Acquisition ◽  
Simplex Virus

ObjectivesTo investigate whether observational studies of HIV and herpes simplex virus type 2 (HSV-2) infections have the capacity to assess the HIV/HSV-2 epidemiological synergy.MethodsAn individual-based Monte Carlo model was used to simulate HIV/HSV-2 epidemics in two scenarios: no HIV/HSV-2 biological interaction and HSV-2 seropositivity enhancing HIV acquisition. Cross-sectional observational studies were simulated by sampling individuals from the population to assess resulting crude and adjusted ORs of the HIV/HSV-2 association. Meta-analyses were conducted to estimate the pooled mean ORs. Impact of under-reporting of sexual behaviour and miscapture of high-risk individuals was assessed through sensitivity analyses.ResultsAssuming no HIV/HSV-2 biological interaction, the crude HIV/HSV-2 OR ranged between 1.38 and 9.93, with a pooled mean of 6.45 (95% CI 5.81 to 7.17). Adjustment for the number of sexual partners over last year, over lifetime and for both partner numbers simultaneously reduced the mean OR to 5.45 (95% CI 4.90 to 6.06), 3.70 (95% CI 3.32 to 4.12) and 3.54 (95% CI 3.17 to 3.94), respectively. Assuming HIV/HSV-2 biological interaction, the crude OR ranged between 3.44 and 9.95, with a pooled mean of 8.05 (95% CI 7.14 to 9.07). The adjustments reduced the mean OR to 7.00 (95% CI 6.21 to 7.90), 3.76 (95% CI 3.32 to 4.25) and 3.68 (95% CI 3.25 to 4.17), respectively. Under-reporting of partners reduced the confounder-adjustment effects. Miscapture of high-risk individuals considerably lowered the estimated ORs.ConclusionsIt is difficult to control for sexual-behaviour confounding in observational studies. The observed HIV/HSV-2 association appears more consistent with two infections sharing the same mode of transmission, rather than with HSV-2 enhancing HIV acquisition.

1352 MICRORNA-MEDIATED TARGETING OF ONCOLYTIC HERPES SIMPLEX VIRUS-1 TO HIGH-RISK BLADDER CANCER

2011 ◽  
Vol 185 (4S) ◽  
Author(s):  
Yoshiyuki Matsui ◽  
Kevin Zhang ◽  
Cleo Lee ◽  
Lisa Skinner ◽  
Javad Banani ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
High Risk ◽  
Herpes Simplex Virus 1 ◽  
Oncolytic Herpes Simplex Virus ◽  
Simplex Virus

Assembly of VP26 in herpes simplex virus-1 capsid implicated by 3-D structure of recombinant capsid

1995 ◽  
Vol 53 ◽  
pp. 840-841
Author(s):  
Z. Hong Zhou ◽  
Jing He ◽  
Joanita Jakana ◽  
J. D. Tatman ◽  
Frazer J. Rixon ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
3D Structure ◽  
Structure Study ◽  
Herpes Simplex Virus 1 ◽  
Shell Proteins ◽  
Life Threatening ◽  
Infected Cells ◽  
Simplex Virus ◽  
Hsv 1

Herpes simplex virus-1 (HSV-1) is a ubiquitous virus which is implicated in diseases ranging from self-curing cold sores to life-threatening infections. The 2500 Å diameter herpes virion is composed of a glycoprotein spike containing, lipid envelope, enclosing a protein layer (the tegument) in which is embedded the capsid (which contains the dsDNA genome). The B-, and A- and C-capsids, representing different morphogenetic stages in HSV-1 infected cells, are composed of 7, and 5 structural proteins respectively. The three capsid types are organized in similar T=16 icosahedral shells with 12 pentons, 150 hexons, and 320 connecting triplexes. Our previous 3D structure study at 26 Å revealed domain features of all these structural components and suggested probable locations for the outer shell proteins, VP5, VP26, VP19c and VP23. VP5 makes up most of both pentons and hexons. VP26 appeared to bind to the VP5 subunit in hexon but not to that in penton.

Ultraviolet Light Induces Reactivation in a Murine Model of Cutaneous Herpes Simplex Virus-1 Infection¶

2001 ◽  
Vol 74 (1) ◽  
pp. 108 ◽  
Author(s):  
Diane E. Goade ◽  
Robert A. Nofchissey ◽  
Donna F. Kusewitt ◽  
Brian Hjelle ◽  
John Kreisel ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Ultraviolet Light ◽  
Murine Model ◽  
Herpes Simplex Virus 1 ◽  
Simplex Virus

scholarly journals Engagement of the Lysine-Specific Demethylase/HDAC1/CoREST/REST Complex by Herpes Simplex Virus 1

2009 ◽  
Vol 83 (9) ◽  
pp. 4376-4385 ◽  
Author(s):  
Haidong Gu ◽  
Bernard Roizman
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Nuclear Bodies ◽  
Wild Type Virus ◽  
Viral Dna ◽  
Herpes Simplex Virus 1 ◽  
Lysine Specific Demethylase ◽  
Repressor Complex ◽  
Infected Cells ◽  
Simplex Virus

ABSTRACT Among the early events in herpes simplex virus 1 replication are localization of ICP0 in ND10 bodies and accumulation of viral DNA-protein complexes in structures abutting ND10. ICP0 degrades components of ND10 and blocks silencing of viral DNA, achieving the latter by dislodging HDAC1 or -2 from the lysine-specific demethylase 1 (LSD1)/CoREST/REST repressor complex. The role of this process is apparent from the observation that a dominant-negative CoREST protein compensates for the absence of ICP0 in a cell-dependent fashion. HDAC1 or -2 and the CoREST/REST complex are independently translocated to the nucleus once viral DNA synthesis begins. The focus of this report is twofold. First, we report that in infected cells, LSD1, a key component of the repressor complex, is partially degraded or remains stably associated with CoREST and is ultimately also translocated, in part, to the cytoplasm. Second, we examined the distribution of the components of the repressor complex and ICP8 early in infection in wild-type-virus- and ICP0 mutant virus-infected cells. The repressor component and ultimately ICP8 localize in structures that abut the ND10 nuclear bodies. There is no evidence that the two compartments fuse. We propose that ICP0 must dynamically interact with both compartments in order to accomplish its functions of degrading PML and SP100 and suppressing silencing of viral DNA through its interactions with CoREST. In turn, the remodeling of the viral DNA-protein complex enables recruitment of ICP8 and initiation of formation of replication compartments.

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