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Biomedical subjects

L R Stanberry

Publications and source records attributed to L R Stanberry.

At least 91 records · Page 5Linked to original sources
PubMed1988

Evaluation of varicella-zoster antiviral drugs by a nucleic acid hybridization assay.

A simple nucleic acid hybridization assay was developed for the evaluation of antiviral compounds with activity against varicella-zoster virus. Antiviral-induced reduction in varicella-zoster virus DNA, as measured by hybridization with 32P-labeled probes, correlated with drug-induced inhibition of viral cytopathic effect in cell culture. Three compounds were shown to be more potent than acyclovir at inhibiting varicella-zoster virus in vitro.

Acyclovir↗
PubMed1988

Herpes simplex virus glycoprotein treatment of recurrent genital herpes.

We investigated the possibility that herpes simplex virus (HSV) glycoproteins might provide potential immunotherapy for recurrent HSV disease by using the guinea pig model of genital HSV infection. In two experiments, after recovery from initial genital herpes, 58 animals were randomized either to receive a glycoprotein vaccine or to serve as controls. Both a mixture of HSV-2 glycoproteins derived from infected tissue cultures and a mixture of HSV-1 glycoproteins B and D, prepared by genetic engineering in mammalian cells, reduced the frequency (P less than .05) and severity (P less than .05) of subsequent herpetic recurrences. We conclude that recurrences of established herpesvirus disease may be altered by administering immunogenic viral proteins; thus, HSV glycoproteins may be useful as immunotherapeutic agents for controlling recurrent HSV infection in humans.

Animals↗
PubMed1988

Antibody to herpes simplex virus (HSV) ICP-35 proteins after HSV challenge of animals immunized with HSV subunit vaccines.

The serological response to the ICP-35 group of herpes simplex virus type 2 (HSV-2) proteins was examined 30 d after vaginal challenge with HSV-2 of guinea pigs previously immunized with HSV glycoproteins. Detection of antibodies to ICP-35 proteins correlated best with the magnitude of vaginal viral replication. Animals that developed antibody to ICP-35 proteins had more-frequent recurrences (P less than .0002) that were of longer duration (P less than .005) than animals that did not. By covariate analysis the number of recurrences appeared to be related to the severity of the acute disease, inversely related to the enzyme-linked immunosorbent assay titer of antibody to HSV glycoproteins, and related to the detection of antibody to ICP-35 proteins. The duration of recurrent disease, however, could only be correlated with the presence of antibody to ICP-35 proteins. Detection of antibody to ICP-35 proteins is thus a useful prognostic indicator for identifying animals that developed more-severe recurrent disease.

Acute Disease↗
PubMed1987

Varicella in a gorilla.

Naturally occurring varicella was observed in a young gorilla in captivity. The isolate was demonstrated to be varicella-zoster virus by restriction enzyme analysis.

Animals↗
PubMed1987

Vaccination with recombinant herpes simplex virus glycoproteins: protection against initial and recurrent genital herpes.

The natural history of initial and subsequent recurrent herpes simplex virus (HSV) genital infection was studied in guinea pigs immunized with HSV glycoprotein vaccines before vaginal challenge with HSV-2. The vaccines used included HSV-1 glycoprotein B and HSV-1 glycoprotein D, both prepared by recombinant DNA techniques, and mixtures of HSV-1 or HSV-2 glycoproteins, prepared from infected cell monolayers by lectin chromatography. Immunizing guinea pigs with subunit HSV glycoprotein vaccines favorably altered the clinical and virological course of initial infection and substantially reduced the incidence, frequency, and duration of recurrent herpetic infections. The extent of protection was influenced by the nature of the glycoprotein vaccine, the immunizing dose, and the co-administration of adjuvant.

Animals↗
PubMed1987

Antibody response to herpes simplex virus glycoprotein D: effects of acyclovir and relation to recurrence.

We developed an enzyme-linked immunosorbent assay (ELISA) for measuring the antibody response to herpes simplex virus (HSV) glycoprotein D (gD). The ELISA was specific and more sensitive than immunoblotting techniques. Antibody to HSV gD was detected in 10 of 12 sera (geometric mean titer, 36.3) obtained from HSV-2-infected guinea pigs 14 days after intravaginal inoculation, and the titer increased to greater than or equal to 5,120 on day 60. Therapy with acyclovir delayed and diminished the antibody response to gD, although by day 60 the titers of antibody to gD in acyclovir-treated animals were not significantly different from those in controls. An increased titer of antibody to gD seemed to be associated with a reduced number of recurrent episodes and to a reduced number of days with recurrent lesions.

Acyclovir↗
PubMed1986

Evaluation of the herpes simplex virus antiviral activity of pyrethrins.

Pyrethrins, complex esters extracted from Chrysanthemum cinerariaefolium, exhibit only minimal in vitro activity against herpes simplex virus (HSV). Employing a guinea pig model of HSV genital infection, no in vivo activity could be demonstrated. Although purported to be an effective remedy for the treatment of genital herpes, we were unable to demonstrate efficacy for either the oral administration of an alcoholic solution of pyrethrins or the topical application of pyrethrins in mineral oil.

Administration, Oral↗
PubMed1986

Genital reinfection after recovery from initial genital infection with herpes simplex virus type 2 in guinea pigs.

The natural history of genital reinfection with herpes simplex virus type 2 (HSV-2) three weeks to one year after initial infection was explored by using a guinea pig model. Intravaginal reinoculation with HSV-2 of animals that had recovered from initial genital infection produced by wild-type or thymidine kinase-deficient HSV-2 produced asymptomatic genital reinfection characterized by high-titered replication of HSV-2 in the vaginal vault. Reinoculation did not result in acute neural infection, as was seen during initial genital herpes, and no evidence of latent infection by the rechallenge strain could be demonstrated. The frequency of recurrences appeared to be established by the initial infection because reinfection did not alter the pattern of recurrent genital herpes. The present study suggest that asymptomatic reinfection may produce a reservoir of communicable virus and that initial infection with a less virulent mutant of HSV-2 may provide protection against subsequent reexposure to wild-type HSV-2.

Animals↗
PubMed1986

Antibody response, recurrence patterns and subsequent herpes simplex virus type 2 (HSV-2) re-infection following initial HSV-2 infection of guinea-pigs: effects of acyclovir.

The production of antibody to specific herpes simplex virus type 2 (HSV-2) polypeptides, the recurrence patterns and the susceptibility to re-infection were studied in the guinea-pig model of genital HSV-2 infection. Further, we defined the effects of acyclovir (ACV) therapy on these parameters of infection. Treatment with ACV reduced the clinical severity of the initial disease but did not affect vaginal viral shedding. Production of neutralizing antibody as well as antibody to the nucleocapsid protein, and glycoproteins B, D and G were all delayed in ACV recipients. ACV treatment of initial infection did not significantly alter the pattern of subsequent recurrence although by several criteria treated animals tended towards decreased recurrences. Re-inoculation with a second strain of HSV-2 resulted in a local cervicovaginal infection but, except for one ACV-treated animal, neural tissue was protected from re-infection.

Acyclovir↗
PubMed1986

Zosteriform spread of herpes simplex virus type 2 genital infection in the guinea-pig.

A model of herpes simplex virus type 2 (HSV-2) infection was developed in the guinea-pig that permits investigation of the role of neural spread of virus in the pathogenesis of genital skin disease. After HSV-2 inoculation of an abraded area lateral to the external genital skin, virus was first detected in the ipsilateral (to the inoculation site) peripheral nerves or genital skin on day 2 or 3 post-inoculation followed by detection in the ipsilateral dorsal root ganglia and spinal cord on day 3 or 4. Virus also spread to the contralateral dorsal root ganglia, contralateral peripheral nerves and contralateral genital skin on day 4 or 5 although lesions were only rarely detected on the contralateral side. Genital skin lesions first developed on day 5 and were followed by the development of lesions along the medial aspect of the ipsilateral hindlimb. Virus was first detected in the vaginal vault on day 4 or 5. The development of lesions appeared to be unrelated to vaginal virus replication but was associated with the recovery of virus from peripheral nerves. Recurrent genital skin lesions were seen more commonly on the inoculated side than the contralateral side. Since the development of skin lesions appeared to result from virus emerging from nerve endings, an event similar to the terminal event that is believed to be involved in the development of recurrent lesions, we now have a model which may be useful in further exploring the pathogenesis of herpetic disease.

Animals↗
PubMed1985

Varicella-zoster virus infection of strain 2 guinea pigs.

Weanling strain 2 guinea pigs are susceptible to infection with varicella-zoster virus cultured in embryonic guinea pig tissue. Animals inoculated by an intramuscular route develop mononuclear cell viremia that may persist for as long as three weeks. During the period of viremia, virus may be recovered from the nasopharynx and a variety of tissues. In addition, virus may be recovered from neural tissues in the absence of viremia, although infectious virus has not been cultivated from neural tissues after the 23rd day. The strain 2 guinea pig should provide an animal model to study the pathophysiology of infections caused by varicella-zoster virus.

Animals↗
PubMed1985

Thymidine kinase-deficient herpes simplex virus type 2 genital infection in guinea pigs.

In guinea pigs, thymidine kinase-producing strains of herpes simplex virus type 2 replicated to high titer in the vagina and spinal cord, and animals developed severe clinical disease. Infection with thymidine kinase-deficient virus resulted in similar vaginal virus titers; however, animals exhibited little or no clinical illness and only low titers of virus were detected in spinal cord homogenate cultures. Neural and extraneural latent infection as well as recurrent infection were noted in animals inoculated with either thymidine kinase-producing or -deficient viruses. These data suggest that neural pathways are important in the pathogenesis of genital herpes and that virus-coded thymidine kinase may influence virulence but is not required for latency.

Animals↗
PubMed1985

Recurrent genital herpes simplex virus infection in guinea pigs.

After recovery from initial genital herpes simplex virus (HSV) infections, female guinea pigs developed spontaneous recurrent infections characterized by discrete erythematous or vesicular herpetic lesions on the external genital skin. HSV type 2 (HSV2) caused significantly more recurrent infections in guinea pigs than did HSV type 1 (HSV1). HSV2-infected animals demonstrated a significant decline in frequency of recurrences over time. The viral nature of the recurrent lesions was confirmed by recovery of infectious HSV, detection of HSV antigen, and histologic examination. Latent HSV2 could be demonstrated in dorsal root ganglia and external genital skin after recovery from the primary infection. Recurrent genital HSV infection in the guinea pig shares many features with recurrent genital herpes in humans and provides a model for studying the relationship between latency and recurrences and for exploring methods for control of recurrent disease.

Animals↗
PubMed1984

More rapid isolation of herpes simplex virus in a continuous line of mink lung cells than in Vero or human fibroblast cells.

Herpes simplex virus (HSV) was isolated from clinical specimens more rapidly in mink lung (ML) cells, a continuous cell line available from a commercial supplier, than in Vero cells or human fibroblast (HF) cells. Stock strains of HSV type 1 (HSV-1) and HSV-2 titered higher in ML cells than in Vero or HF cells. ML cells were equivalent to rabbit kidney (RK) cells in the isolation of HSV in clinical specimens, but titers of stock HSV strains were lower. ML cells could be employed to type strains of HSV-1 and HSV-2, using the technique of differential susceptibility to bromovinyldeoxyuridine (BVDU). ML cells, therefore, are a convenient and useful cell line for the isolation and typing of HSV in diagnostic virology laboratories.

Animals↗
PubMed1983

Photoperiodic control of melanoma growth in hamsters: influence of pinealectomy and melatonin.

Pinealectomy (PX) increased MM1 (melanotic melanoma no. 1) hamster melanoma growth in animals held under a 14-h light, 10-h dark (14:10) photoperiod without altering tumor latency. Hamsters maintained under a 6-h light, 18-h dark (6:18) photoperiod exhibited gonadal collapse, a longer tumor latency, and slower tumor growth rate than animals held under 14:10. PX produced a further increase in tumor latency and a decrease in growth in these animals. In contrast, acute morning injection of low doses (50 micrograms/day) of melatonin or delivery by Silastic capsule (35 micrograms/day) implanted at the time of tumor cell inoculation increased MM1 melanoma growth in hamsters held under 14:10 photocycle, without affecting testicular or adrenal function. Treatment of hamsters 11 weeks before tumor cell inoculation with 14 micrograms/day melatonin via Silastic capsule produced a decrease in serum PRL but no change in tumor growth or testicular or adrenal weights in animals held under 14:10. Treatment of hamsters with 17.7 micrograms/day melatonin (Silastic capsule) 11 weeks before tumor cell inoculation increased testes and adrenal weights as well as serum PRL and androgen levels, but significantly decreased tumor growth in hamsters held under a short daily photoperiod. These results suggest that the photoperiod under which hamsters are maintained dictates the growth rate of MM1 tumors and the effect of PX on tumor behavior. When photoperiod significantly alters gonadal and adrenal function, the quantity, time, and duration of melatonin presentation are all important variables in the effect of melatonin on tumor growth.

Adrenal Glands↗
PubMed1982

Genital herpes in guinea pigs: pathogenesis of the primary infection and description of recurrent disease.

Guinea pigs inoculated intravaginally with herpes simplex virus type 2 (HSV-2) developed a self-limiting infection characterized by vesiculo-ulcerative lesions on the external genital skin, urinary retention, and hindlimb paralysis. Infection rarely resulted in death. Virologic, histologic, and immunoperoxidase data suggested the following scheme for viral pathogenesis: initial replication in the introitus, vagina, and bladder; spread via sensory nerves to the lumbosacral dorsal root ganglia and spinal cord, and transmission via peripheral nerves to the external genital skin to produce the characteristic lesions. After recovery from primary infection, animals developed recurrent vesicular lesions, shed virus from genital sites in the absence of lesions, and harbored latent HSV-2 in dorsal root ganglia. Genital infection in the guinea pig shares many features with genital herpes in humans and provides a model to explore mechanisms of latency and reactivation and to evaluate several methods for control of recurrent disease.

Animals↗
PubMed1982

Biological behavior of MM1 hamster melanoma.

We have reported evidence recently for a high-affinity receptor for glucocorticoid Malignant Melanoma No. 1 hamster melanoma and suggested that tumor growth was facilitated by adrenal steroids. This report characterizes the behavior of Malignant Melanoma No. 1 following manipulation of the pituitary-adrenal axis in vivo. Bilateral adrenalectomy significantly retarded tumor growth. Hypophysectomy also significantly reduced tumor growth. Silastic implants of hydrocortisone in intact hamsters produced a dose (7 to 28 micrograms/day)-related increase in tumor growth. Implants releasing a low dose (3 micrograms/day) of dexamethasone also increased tumor growth. Chronic exposure of adrenalectomized and intact hamsters to a high dose (125 micrograms/day) of desoxycorticosterone acetate also produced a significant increase over adrenalectomized and sham-adrenalectomized controls. In contrast, chronic administration of adrenocorticotropic hormone and alpha-melanocyte-stimulating hormone to intact hamsters did not significantly alter melanoma growth. These observations support the suggestion that adrenocorticosteroids influence the growth of Malignant Melanoma No. 1 hamster melanoma and provide a model for studying the regulation of growth of a glucocorticoid-positive neoplasm originating outside the reticuloendothelial system.

Adrenalectomy↗