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At least 235 records · Page 13Linked to original sources
PubMed2005

Spectroscopic analysis of Kaposi's sarcoma-associated herpesvirus infected cells by Raman tweezers.

Kaposi's sarcoma-associated herpesvirus (KSHV), also referred to as human herpesvirus-8 (HHV-8), is a tumor causing virus. KSHV is the cause of several disease conditions known as Kaposi's sarcoma, multicentric Castleman disease, and primary effusion lymphoma. Cell culture supernatants from KSHV infected hematopoietic cells induced angiogenic tubule formation to a significantly greater extent than uninfected hematopoietic cells. Raman spectrum profiles were generated to differentiate the uninfected from KSHV infected cells. In general, profiles from all the hematopoietic cells shared similar peaks; however, the relative abundance of specific components varied significantly between the cells. Subsequent use of the multivariate analysis of the Raman spectra revealed significant differences between the uninfected and the KSHV infected cells. Taken together, this study reports the use of Raman tweezers to distinguish and analyze the biological relevance of KSHV infected cell signaling.

Animals↗
PubMed1993

Central nervous system herpesvirus infection in systemic lupus erythematosus: diagnosis by endoretinal biopsy.

A 31-year-old woman with systemic lupus erythematosus (SLE) developed meningoencephalitis, followed by transverse myelitis. The clinical picture was otherwise not consistent with a lupus flare. Extensive diagnostic evaluation was unrevealing. Acute visual loss ensued, associated with an unusual pattern of retinitis. Endoretinal biopsy established the diagnosis of herpesvirus infection. Reinstitution of antiviral therapy, and optic nerve sheath decompression, led to resolution of neurologic deficits and partial return of vision. Our report is the first that describes a patient with SLE with herpes meningoencephalitis, transverse myelitis, and rapidly progressive outer retinal necrosis, diagnosed antemortem by endoretinal biopsy, and successfully treated with acyclovir and optic nerve fenestration.

Acyclovir↗
PubMed1999

Cellulose acetate phthalate (CAP): an 'inactive' pharmaceutical excipient with antiviral activity in the mouse model of genital herpesvirus infection.

The spread of sexually transmitted infections caused by herpes simplex virus type 2 (HSV-2) has continued unabated. At least 20% of the United States population has been infected with HSV-2 and there is a high probability of further virus transmission by asymptomatic carriers. Given the absence of effective vaccines, this indicates the need to develop prophylactic measures such as topical microbicides that have antiviral activity. Recent studies indicate that cellulose acetate phthalate (CAP), an inactive pharmaceutical excipient commonly used in the production of enteric tablets and capsules, is a broad specificity microbicide against diverse sexually transmitted pathogens. When appropriately formulated in micronized form, it inactivates various viruses, including HSV-2, in vitro. Here we show that CAP inhibits HSV-2 infection in the mouse model of genital HSV-2 infection. Pretreatment with micronized CAP formulated in a glycerol-based cream with colloidal silicone dioxide significantly reduced the proportion of HSV-2-infected mice (10% virus shedding, 0-5% lesion development and 0% fatality for CAP as compared to 84% shedding, 63% lesion development and 63% fatality in saline-treated mice). These differences were significant (P < or = 0.0002 by the test of equality of two proportions). Virus titres in the minority of mice that developed infection were similar to those in untreated mice. HSV-2 infection was not inhibited by treatment with CAP formulated with other inactive ingredients (for example povidone plus crosprovidone) instead of silicone dioxide, presumably reflecting CAP complexation/inactivation. These data suggest that properly formulated, CAP may be an efficacious agent for preventing vaginal transmission of genital herpesvirus infections.

Animals↗
PubMed1977

Cellular immunity and herpesvirus infections in cardiac-transplant patients.

We observed severe infection with herpes simplex virus in cardiac-transplant patients despite their high serum antibody levels to this virus. Therefore, we sought to correlate clinical susceptibility to two herpesvirus (simplex and zoster) infections with specific cellular immunity, assessed by the transformation and interferon responses of peripheral blood mononuclear cells to heat-inactivated antigens. Transformation and interferon response to herps simplex virus was maximally depressed immediately after transplantation, the time when severe and prolonged infection with herps simplex virus occurred. Six months to six years after transplantation, both clinical susceptibility and cellular immunity to herpes simplex virus were normal. Herpes zoster infections were more frequent than normal at all times after cardiac transplantation; depressed or absent cellular responses to the varicella zoster virus paralleled that susceptibility. In these patients the risk of severe herpesvirus infections correlated with depressed cellular immune responses to the specific viral agent involved.

Antibodies, Viral↗
PubMed1982

Enzymatic deoxyglucosylation of ceramides by microsomes of BHK-21 cells. The effect of deoxyglucose treatment and herpesvirus infection.

The microsomal fractions of cultured hamster fibroblasts (BHK-21 cells) catalyze the incorporation of glucose from UDPglucose or of deoxyglucose from UDPdeoxyglucose into a reaction mixture with liposomes consisting of ceramide and phosphatidylcholine. The microsomal fractions also catalyze the transfer of glucose from UDPglucose to endogenous acceptors. The specific activity of ceramide deoxyglucoside or ceramide glucoside formation was significantly higher when microsomal preparations obtained from deoxyglucose-treated or herpesvirus-infected BHK-21 cells were used as the glucosyltransferase source. Deoxyglucose was incorporated from UDPdeoxyglucose into hydroxy- and nonhydroxy-fatty acid-containing ceramides at approximately the same rate. Competitive inhibition of deoxyglucosylation of ceramides by UDPglucose suggests that both reactions were catalyzed by the same enzyme, viz. UDPglucose:ceramide glucosyltransferase. This inhibition of glycosphingolipid synthesis may account, in part, for the inhibitory effect of deoxyglucose on lipid-containing viruses.

Animals↗
PubMed1997

[Herpesvirus infections in free living black tufted ear marmosets (Callithrix penicillata, E. Geoffroyi 1812) at the State Park of Serra da Tiririca, Niterói, Rio de Janeiro, Brazil].

The mortal cause of black-tufted-ear marmoset (Callithrix penicillata), living in a conservation unit of State Park of Serra da Tiririca-Niterói-RJ, Brasilien, has been investigated in 1995 based on different examinations realized in one animal. After clinical, light and electron microscopic investigations, herpesvirus infection was found to be the etiological agent of the disease.

Animals↗
PubMed1983

Phase I evaluation of 2'-fluoro-5-iodo-1-beta-D-arabinofuranosylcytosine in immunosuppressed patients with herpesvirus infection.

2'-Fluoro-5-iodo-1-beta-D-arabinofuranosylcytosine (FIAC) is a potent selective inhibitor of the replication of herpes simplex virus types 1 and 2 (HSV-1, HSV-2), varicella zoster virus, and cytomegalovirus in cell culture systems. FIAC produces an unequivocal therapeutic effect in mice that have been inoculated with a lethal burden of HSV-1. We have administered FIAC to 32 host compromised patients, 30 with advanced cancer, who were experiencing acute herpesvirus infections (varicella zoster, 29; HSV-1, 2; HSV-2, 1); the drug was given by 20 min i.v. infusion twice a day for 7 days. The dosage levels explored were 60, 120, 240, 400, and 600 mg/sq m/day. Drug-induced myelosuppression became evident at 600 mg/sq m/day; thrombocytopenia exceeded leukopenia. The toxic low dose was 400 mg/sq m/day with mild nausea and rare myelosuppression. All 24 varicella zoster patients with cutaneous disease receiving FIAC, greater than or equal to 120 mg/sq m/day, experienced stabilization of cutaneous lesions within 48 to 72 hr; healing began promptly thereafter.

Antiviral Agents↗
PubMed1993

Systemic antivirals in herpesvirus infections.

Over the last few years we have seen the advent of effective antiviral drug therapy, the major ramifications being in the area of herpes infections. Acyclovir has become an established part of clinical practice, and other compounds are being increasingly used in the immunocompromised host. An effective vaccine is available for chickenpox, but herpes simplex and cytomegalovirus vaccines are still in early development. Thus, antiviral agents will continue to play a major role in the management of all herpesvirus infections for the foreseeable future. Current work includes the development of increased bioavailability prodrugs (BW 256, famciclovir), which are converted to active drug once absorbed, enabling rapid high serum levels, and hence may turn out to have increased efficacy in HSV- and VZV-induced diseases, for which oral acyclovir currently is the treatment of choice. Markedly increased efficacy against VZV in vitro has been demonstrated by two current agents under study (BVaraU, BW 882). HPMPC is now entering clinical trials with a markedly improved efficacy profile against CMV and HSV in animal models. Finally, drug combinations that are being investigated in AIDS may offer a means to avoid resistance in herpes infections in immunocompromised patients.

Acquired Immunodeficiency Syndrome↗
PubMed1981

Herpesvirus infection enhances cholesterol and cholesteryl ester accumulation in cultured arterial smooth muscle cells.

In our previous experiments, atherosclerosis similar to that in humans was reproducibly induced in both normocholesterolemic and hypercholesterolemic specific-pathogen-free (SPF) chickens by infection with Marek's disease herpesvirus (MDV). In contrast, uninfected chickens fed either relatively cholesterol-poor or cholesterol-supplemented diets did not develop this arterial disease. In experiments reported here, the hypothesis that infection of arterial smooth muscle cells (SMCs) with MDV would enhance lipid accumulation in these cells was tested. The number of MDV-infected SMCs with lipid stained with oil red O was assessed, and the lipid content of these cells was quantitated chemically by chromatographic and fluorometric analyses. These data were compared to those of uninfected control cells and, in the case of chemical analyses, were also compared to SMCs infected with a second avian herpesvirus, turkey herpesvirus (HVT). Results indicate the following: 1) The percentage of MDV-infected SMCs containing stainable lipid was significantly greater than the percentage of uninfected SMCs; 2) Increased total lipid accumulation was observed in MDV-infected SMC, particularly cholesterol (CH) and cholesteryl esters (CEs), as compared with uninfected or HVT-infected cells; 3) The types of CEs and nonesterified fatty acids (NEFA) accumulating in MDV-infected cells (particularly saturated types of CEs and NEFAs) were significantly different than those in uninfected or HVT-infected SMCs. These qualitative and quantitative differences in lipid content between infected and uninfected SMCs suggest that infection with MDV results in altered intracellular lipid metabolism. Results support the hypothesis that lipid accumulation in arteries of normocholesterolemic chickens may result from MDV infection acting at the cellular level to induce lipid accumulation that resembles that in human atheroarteriosclerosis.

Animals↗
PubMed1993

Biological response modifier-mediated resistance to herpesvirus infections requires induction of alpha/beta interferon.

The role of interferon alpha/beta (IFN) induction by the immunomodulators pICLC and CL246,738 was investigated in CD-1 mice infected with murine cytomegalovirus (MCMV) or herpes simplex virus type 2 (HSV-2). Mice were treated with either normal sheep serum or anti-alpha/beta IFN antiserum, inoculated with the immunomodulators, and infected with virus. Because anti-IFN treatment also decreased natural resistance to HSV-2 and MCMV, two viral challenge doses were used to ensure that the mice with control serum or anti-IFN antiserum received biologically equivalent infections. Antiviral protection of pICLC and CL246,738 against HSV-2 infection was completely abrogated by treatment with anti-alpha/beta interferon antiserum. Mice treated with pICLC also lost antiviral protection against MCMV when interferon alpha/beta was depleted. These results indicate that induction of interferon alpha/beta appears to be a major mechanism for both natural resistance and pICLC-induced antiviral protection against MCMV and HSV-2 herpesvirus infections.

Acridines↗
PubMed1977

Prospective study of prevalence, incidence, and source of herpesvirus infections in patients with renal allografts.

The prevalence, incidence, and source of infections with different types of herpesviruses were determined prospectively for 25 persons undergoing hemodialysis, 30 allograft recipients, and 16 kidney donors. The prevalence of prior infections with cytomegalovirus (CMV), herpes simplex virus (HSV), and Epstein-Barr virus (EBV) was high (72%-100%) and was similar for healthy persons and those with renal failure. The incidence of infections in patients undergoing hemodialysis was no greater than that before dialysis. In allograft recipients, the incidence of infection with CMV was 73%; HSV, 57%; EBV, 30%; and varicella-zoster virus (clinical), 7%. Ninety-seven percent of the patients developed an infection with one or more herpesviruses. Transfusions, hemodialysis, the allograft, and hospital environment were not significant sources in transmission. Uremia and splenectomy were unimportant in the reactivation of infection. Immunosuppressive drugs possibly algmented by a graft rejection response account for the high incidence of recrudescent infections with CMV and HSV.

Adult↗
PubMed1980

Cimetidine in the treatment of herpesvirus infections.

In August 1977 a patient developed herpes zoster just before she commenced a course of cimetidine (Tagamet; Smith, Kline & French) for a chronic gastric ulcer. She experienced both rapid relief of the ulcer symptoms and, rather unexpectedly, dramatic relief of the herpetic pain and rapid disappearance of the eruption. On the basis of this observation cimetidine was prescribed to 21 patients with herpes zoster. The results continued to be encouraging in all but 3 patients. The trial was therefore extended to other herpesvirus infections. In all but 1 of 7 patients with herpes labialis the blisters were aborted, and in 1 patient with herpes keratitis the result was also encouraging, the attacks being markedly shortened in duration and reduced in frequency. The results of this preliminary trial warrant a systematic scientific inquiry into the potential role of cimetidine in the treatment of hypesvirus infection, as well as a study of the mechanisms involved.

Adolescent↗
PubMed1983

Induction of generalized and lethal herpesvirus infection in the tree shrew by intrahepatic transfection of herpes simplex virus DNA.

The infectivity of herpes simplex virus (HSV) genome was investigated in vivo using the tree shrew, which is highly susceptible to HSV, as an animal model. Individual tree shrews were inoculated intrahepatically with 0.2 ml of a transfection mixture containing 25 micrograms HSV DNA, 50 micrograms salmon sperm DNA, and 250 micrograms DEAE-dextran. Seven out of nine tree shrews transfected with HSV DNA developed a generalized herpesvirus infection. The new virus progeny was found in different organs of transfected animals.

Animals↗
PubMed1976

Disseminated herpesvirus infection. Association with primary genital herpes in pregnancy.

A patient with primary herpes simplex virus (HSV) type 2 genital infection had dissemination in the 37th week of her first pregnancy. This was manifested by severe hepatitis, pancreatitis, and genital lesions. Temporary improvement followed the delivery of a healthy infant by cesarean section. Encephalitis became evident on the third postpartum day, and recovery was complicated by profound bradycardia, possibly due to viral myocarditis. Vidarabine was administered for seven days, and the patient survived with only mild neurologic sequellae. To our knowledge, this the fourth reported case of disseminated herpesvirus infection in pregnancy and the first due to HSV type 2. Pregnancy must be considered as a possible predisposing factor in dissemination of primary HSV infection.

Adult↗
PubMed2004

Raf-induced vascular endothelial growth factor augments Kaposi's sarcoma-associated herpesvirus infection.

Recombinant green fluorescent protein encoding Kaposi's sarcoma-associated herpesvirus (rKSHV.152) infection of beta-estradiol stimulated human foreskin fibroblasts (HFF) or HFF/DeltaB-Raf([FF]):ER (expressing a weaker form of B-Raf) could be enhanced to levels comparable to that of HFF/DeltaB-Raf([DD]):ER cells by pretreating cells with soluble vascular endothelial growth factor (VEGF). Conversely, VEGF expression and infection efficiency typically observed in beta-estradiol stimulated HFF/DeltaB-Raf([DD]):ER cells could be lowered significantly by treating with VEGF small interfering RNA. In addition, we observed enhancement of the KSHV infection in HFF cells transfected with human VEGF(121). These results confirm the ability of Raf-induced VEGF to augment KSHV infection of cells.

Cells, Cultured↗
PubMed1988

Cytotoxic T lymphocytes. Their relevance in herpesvirus infections.

We have used recombinant vaccinia viruses expressing the cloned genes coding for glycoprotein B (gB) or glycoprotein D (gD) of HSV-1 to analyze the role of HSV-1--specific cytotoxic T lymphocytes (CTL) in antiviral immunity. Various studies in mice revealed that either vector could stimulate some aspects of HSV-1--specific immunity, but surprisingly, HSV-specific CTL were not induced. Even though gD appeared to be a target antigen for class II-MHC-restricted CTL, neither the gB or the gD vector was capable of forming a target-cell complex that was recognized by class I-MHC-restricted HSV-specific CTL. The inability of these major extracellular glycoproteins to act as CTL-target antigens was even more unusual in light of the ability of CTL to apparently recognize the immediate early genes of HSV, none of which are considered to be expressed on the surface of infected cells. The selective failure of either the gB or gD vector to induce numerous aspect of anti-HSV immunity in the absence of a CTL response allowed us to assess the consequence of this failure in terms of the level of protective immunity against HSV challenge seen in vector-immunized mice. These studies suggest that this failure to induce HSV-specific CTL appears to minimize the protective response to only efficiently protecting against low-challenge doses of HSV-1. These findings are discussed with relevance to the role of CTL in the control of herpesvirus infections.

Animals↗
PubMed2006

Asynchronous progression through the lytic cascade and variations in intracellular viral loads revealed by high-throughput single-cell analysis of Kaposi's sarcoma-associated herpesvirus infection.

Kaposi's sarcoma-associated herpesvirus (KSHV or human herpesvirus-8) is frequently tumorigenic in immunocompromised patients. The average intracellular viral copy number within infected cells, however, varies markedly by tumor type. Since the KSHV-encoded latency-associated nuclear antigen (LANA) tethers viral episomes to host heterochromatin and displays a punctate pattern by fluorescence microscopy, we investigated whether accurate quantification of individual LANA dots is predictive of intracellular viral genome load. Using a novel technology that integrates single-cell imaging with flow cytometry, we found that both the number and the summed immunofluorescence of individual LANA dots are directly proportional to the amount of intracellular viral DNA. Moreover, combining viral (immediate early lytic replication and transcription activator [RTA] and late lytic K8.1) and cellular (syndecan-1) staining with image-based flow cytometry, we were also able to rapidly and simultaneously distinguish among cells supporting latent, immediate early lytic, early lytic, late lytic, and a potential fourth "delayed late" category of lytic replication. Applying image-based flow cytometry to KSHV culture models, we found that de novo infection results in highly varied levels of intracellular viral load and that lytic induction of latently infected cells likewise leads to a heterogeneous population at various stages of reactivation. These findings additionally underscore the potential advantages of studying KSHV biology with high-throughput analysis of individual cells.

Antigens, Viral↗
PubMed1983

Evaluation of prodrugs of 9-beta-D-arabinofuranosyladenine for therapeutic efficacy in the topical treatment of genital herpesvirus infections in guinea pigs.

Prodrugs of the antiviral agent 9-beta-D-arabinofuranosyladenine (araA), which were more effective than the parent compound in penetrating vaginal membranes in vitro, were synthesized and examined for efficacy in the topical treatment of genital infections with herpes simplex virus type 2 in female guinea pigs. Treatment with 10% araA-5'-monophosphate or 10% araA-5'-monovalerate twice a day for 7 days, starting 6 h after intravaginal inoculation with virus, completely aborted the primary infection. When initiation of treatment was delayed until 24 h postinfection, araA-5'-monophosphate and araA-5'-monovalerate were no longer effective in reducing the mean lesion scores or mean vaginal virus titers. Treatment with 5% acyclovir, starting at 24 h postinfection, failed to prevent genital lesion development but significantly reduced the peak mean lesion score (approximately 50%). Topical therapy with 10% araA-2',3'-diacetate, initiated at 24 h postinfection, was as effective as, if not more effective than, acyclovir in reducing the severity of herpes genitalis in guinea pigs. Treatment with 10% araA-2',3'-dipropionate or 10% araA-2',3'-dibutyrate was without benefit. Among a series of 5'-monoesters of araA, araA-5'-monobutyrate appeared to be the most effective but was less active than araA-2',3'-diacetate. These data indicate that araA-2',3'-diacetate may be an effective antiviral agent for topical use against genital herpesvirus infections.

Acyclovir↗