Herpes simplex virus type 2 (HSV-2) infection is the most common cause of genital ulcerative disease in the developed world. Antibodies to herpes simplex viral-induced antigens (HSVIA) were assayed by an indirect immunofluorescent technique in 93 regular cigarette smokers, 75 of whom also imbibed alcoholic beverages. During the course of investigating T cell responses to HSV among volunteers entering trials of investigational genital herpes vaccines, 6 of the 24 immunocompetent subjects with no prior history of oral/labial or genital herpes possessed HSV-specific T cell immunity but, by multiple determinants of even the most sensitive serological assays, remained seronegative to HSV-1 and -2. Physical or psychological stress can modulate immune responses in normal subjects. We present data to confirm that exposure to varicella boosts immunity to herpes-zoster. Thirty-four patients, subject to recurrent herpes labialis, have been studied.
The in vitro lymphoproliferative responses to herpes simplex virus (HSV) antigens were followed in rabbits with herpesvirus infection of the cornea. Intravaginal (IVAG) inoculation of wild-type herpes simplex virus type 2 (HSV-2) in mice causes epithelial infection followed by lethal neurological illness, while IVAG inoculation of attenuated HSV-2 causes epithelial infection followed by development of protective immunity against subsequent IVAG challenge with wild-type virus. Herpes simplex virus 1 (HSV-1) causes a spectrum of disease, including herpes labialis, herpes keratitis, and herpes encephalitis, which can be lethal. Immune Design is committed to exploiting the full potential of its product development capabilities. Our research laboratory focuses on two related areas. SEATTLE and SOUTH SAN FRANCISCO, Calif., Oct.
Herpes simplex virus (HSV) is a prevalent neurotropic virus, which establishes lifelong latent infections in the neurons of sensory ganglia. Vitaliano PP, Dougherty CM, Siegler IC: Biopsychosocial risks for cardiovascular disease in spouse caregivers of persons with Alzheimer’s disease. The influence of herpes zoster virus infection on cell-mediated and humoral immunity to varicella-zoster virus (VZV), cytomegalovirus, and herpes simplex virus (HSV) was followed in 17 zoster patients from the first week to 6 months after start of eruptions. HSV-1 and HSV-2 encode gC, a viral complement control protein that inhibits complement activation by binding C3b (Friedman et al., 1984; Kostavasili et al., 1997). Understanding the mechanisms by which herpes simplex virus (HSV) evades host immune defenses is critical to defining new approaches for therapy and prevention. HSV type 1 (HSV-1) has evolved numerous strategies for modifying immune responses that protect against infection.
Herpes simplex virus (HSV) infections impose an enormous health burden on the world’s population with HSV-2 being the leading cause of genital ulcerative disease and contributing to the spread of HIV infections. Administration of herpes simplex thymidine kinase (HSV-tk)-expressing, gene-modified T cells (GMCs) with T cell-depleted bone marrow transplantation (TCD-BMT) can allow modulation of posttransplantation alloreactivity. Herpes simplex virus type 1 (HSV-1) is a naturally neurotropic DNA virus proficient in establishing latent infection within neurons, but moreover possesses the ability to infect a wide range of cell/tissue types. VZV infected MeWo cells showing typical herpes-virus-induced multinucleated giant cells. We report a case of non-immune hydrops fetalis (NIHF) caused by herpes simplex virus type 2 (HSV-2) in an infant whose mother had recurrent HSV-2 infection. The family of viruses known as the herpes viruses – are responsible for a number of different painful infections that often have “latent” or recurring tendencies.
Herpes simplex virus (HSV) is a large DNA virus with unique properties that can be exploited for in vivo gene therapy. Herpes zoster is a common illness that can lead to serious morbidity. Herpes simplex virus (HSV) recombinants and replication-defective HSV mutants are being evaluated as potential genital herpes vaccines (1, 10, 12, 17, 40, 43, 56, 66) and as novel vaccine vectors (50). Herpes simplex virus 1 (HSV-1) establishes lifelong latent infections in the sensory neurons of the trigeminal ganglia (TG), wherein it retains the capacity to reactivate. Oncolytic viruses (OVs), like oncolytic herpes simplex virus (oHSV), are genetically engineered to selectively replicate in and kill cancer cells, while sparing normal cells. Infections with herpes simplex virus type 1 (HSV-1) in humans and in animal models are accompanied by enhanced natural killer (NK) activity.
Herpes simplex viruses are large double-stranded DNA viruses. Depo-provera, a long-acting progestational formulation, is widely used to facilitate infection of sexually transmitted diseases in animal models.