PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “HERPESVIRUS INFECTIONS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 163 records · Page 9Linked to original sources
PubMed1986

An outbreak of a herpesvirus infection in harbor seals (Phoca vitulina).

During an outbreak of a herpesvirus infection in juvenile harbor seals, 11 out of 23 seals died. The duration of the disease in these 11 animals varied from 1-6 days. Nasal discharge, inflammation of the oral mucosa, vomiting, diarrhea and fever up to 40 degrees C were observed in the first days of the disease. In later stages coughing, anorexia and lethargy occurred. Severe necrosis of the liver and interstitial pneumonia were the most striking histopathological findings.

Animals↗
PubMed1978

Serodiagnosis of herpesvirus infection in primates.

The presence of herpesviruses in various animal tissues used for vaccine production is of importance, inasmuch as these viruses may go unrecognized, residing in latent form. Of greatest concern is Herpesvirus simiae (B virus) present in the majority of macaca species, one of the more extensively used laboratory nonhuman primates. The close antigenic relationship of B virus to human herpes strains (H. hominis) and SA8 (a baboon herpesvirus) makes serologic differentiation extremely difficult, but necessary. Complicating the differential diagnosis is the frequent infection of simian species with human strains. The present study clearly shows that many animal sera negative to herpes simplex will be negative to B virus in the neutralization test. However, a sufficient number of sera will be negative to simplex, but positive to B virus, indicating that the assumed one-way cross is invalid. Also, if antibody to simplex is present, and this antibody is present in most adult macaques, then differentiation requires testing with B virus. At least 50% of these positive sera may appear to be negative for B virus if only tested with H. hominis. Approximately 25% of the remaining positive sera will have higher titers to B virus than to herpes simplex and 25% will have the same titers to both viruses. Further, complement is required by many of the test sera to detect the presence of antibodies to B virus.

Animals↗
PubMed1985

Pathologic changes in pigs with prednisolone-induced recrudescence of herpesvirus infection.

In pigs inoculated with Aujeszky's disease virus (ADV), recrudescence of herpesvirus infection was induced by daily administration of 1,000 mg of prednisolone for 5 days at 2 (group A) or 5 (group B) months after the primary infection. At necropsy in group A pigs, ADV was recovered from nasal secretions 3 to 9 days after prednisolone treatment initiation and from the brain cortex 10 days after treatment initiation; ADV was not recovered from group B pigs. In pigs of both groups killed 10 days after treatment initiation, 2 types of characteristic lesions were found. One type was a nonsuppurative encephalitis that consisted of neuronal necrosis, neuronophagia, and formation of eosinophilic intranuclear inclusion bodies. The 2nd type had basophilic intranuclear inclusion bodies in the enlarged endothelial cells of the kidneys, liver, lungs, adrenal glands, and lymph node sinusoids. Cells containing intranuclear inclusion bodies had immature and mature herpesvirus particles. Therefore, the brain lesions containing the eosinophilic inclusion bodies were considered to be due to ADV. Basophilic inclusion bodies in the endothelial cells were due to porcine cytomegalovirus. These observations indicated that prednisolone treatment resulted in recrudescence of ADV and porcine cytomegalovirus infections.

Animals↗
PubMed1990

[New types of virus infections of domestic animals in the German Democratic Republic. 3. Seroepizootiologic and experimental studies of herpesvirus infections in sheep--the etiology of pulmonary adenomatosis].

Neutralisation tests for antibodies against ovine herpesvirus were applied to 848 sera which had been sampled from different sheep herds across the GDR. Between six and 20 percent of sheep in the herds tested exhibited neutralising antibodies, notwithstanding their pulmonary adenomatosis status. Incidence and titre distribution of antibodies against ovine herpesviruses in pulmonary adenomatosis herds were identical with those recorded from unsuspected herds. From among 21 sheep with pathomorphologically secured pulmonary adenomatosis, six animals exhibited antibody titres just as high as those recorded from responders of all herds examined. Lambs were obtained by hysterectomy and raised without mothers and were experimentally infected with Herpesvirus ovis. All of these animals responded to infection by clearly rising titres (between 1:2 and 1:32). Adenomatous pulmonary lesions were not recordable from any of them. One lamb, following experimental ovine herpesvirus infection, exhibition, exhibited subclinical interstitial pneumonia. Herpesvirus ovis has been widespread in sheep herds across the GDR. The authors' serological and experimental investigations do not support the assumption of an aetiological relationship between ovine herpesvirus infection and incidence of pulmonary adenomatosis.

Animals↗
PubMed2003

Latent herpesvirus infection in human trigeminal ganglia causes chronic immune response.

The majority of trigeminal ganglia (TGs) are latently infected with alpha-herpesviruses [herpes simplex virus type-1 (HSV-1) and varicella-zoster virus (VZV)]. Whereas HSV-1 periodically reactivates in the TGs, VZV reactivates very rarely. The goal of this study was to determine whether herpesvirus latency is linked to a local immune cell infiltration in human TGs. T cells positive for the CD3 and CD8 markers, and CD68-positive macrophages were found in 30 of 42 examined TGs from 21 healthy individuals. The presence of immune cells correlated constantly with the occurrence of the HSV-1 latency-associated transcript (LAT) and only irregularly with the presence of latent VZV protein. In contrast, uninfected TGs showed no immune cell infiltration. Quantitative RT-PCR revealed that CD8, interferon-gamma, tumor necrosis factor-alpha, IP-10, and RANTES transcripts were significantly induced in TGs latently infected with HSV-1 but not in uninfected TGs. The persisting lymphocytic cell infiltration and the elevated CD8 and cytokine/chemokine expression in the TGs demonstrate for the first time that latent herpesviral infection in humans is accompanied by a chronic inflammatory process at an immunoprivileged site but without any neuronal destruction. The chronic immune response seems to maintain viral latency and influence viral reactivation.

Adolescent↗
PubMed1983

Lysis of herpesvirus-infected cells by macrophages activated with free or liposome-encapsulated lymphokine produced by a murine T cell hybridoma.

Thioglycolate-induced mouse peritoneal macrophages were activated in vitro by the lymphokine designated macrophage-activating factor (MAF) produced by a murine T cell hybridoma to lyse herpes simplex virus type 2 (HSV-2)-infected murine target cells. Comparison of uninfected BALB/c 10E2 cells with HSV-2-infected 10E2 cells showed that macrophages activated with MAF selectively destroyed HSV-2-infected cells and left uninfected cells unharmed, as measured by an 18-h 51Cr-release assay. In contrast, macrophages treated with medium were as efficient as MAF-activated macrophages in suppressing the production of HSV-2 from virus-infected cells. These findings suggest that macrophages must attain an activated state to lyse HSV-2-infected cells. Finally, incubation of macrophages with liposomes containing MAF was shown to be a highly efficient method for activation of macrophages against HSV-2 infected cells. The ability to selectively destroy herpesvirus-infected cells in vitro by macrophages activated with liposome-encapsulated MAF suggests that the therapeutic efficacy of this treatment in vivo should be evaluated.

Animals↗
PubMed1995

Altered cholesterol trafficking in herpesvirus-infected arterial cells. Evidence for viral protein kinase-mediated cholesterol accumulation.

Herpesvirus infection of arterial smooth muscle cells has been shown to cause cholesteryl ester (CE) accumulation. However, the effects of human herpes simplex virus type 1 (HSV-1) infection on cholesterol binding and internalization, intracellular metabolism, and efflux have not been evaluated. In addition, the effects of viral infection on signal transduction pathways that impact upon cholesterol metabolism have not been studied. We show in studies reported herein that HSV-1 infection of arterial smooth muscle cells enhances low density lipoprotein (LDL) binding and uptake which parallels an increase in LDL receptor steady state mRNA levels and transcription of the LDL receptor gene. HSV-2 also increases CE synthesis and 3-hydroxy- 3-methylglutaryl-CoA reductase activity but concomitantly reduces CE hydrolysis and cholesterol efflux. Interestingly, this viral infection was associated with a time-dependent decrease in protein kinase A activity and an increase in viral-induced protein kinase (VPK) activity commensurate with the accumulation of esterified cholesterol. The relationship between increased VPK activity and alterations in CE accumulation in virally infected cells was explored using an HSV-1 VPK- mutant in which the portion of the HSV-1 genome encoding VPK had been deleted. Cholesteryl ester accumulation was significantly increased (> 50-fold) in HSV-1-infected cells compared to uninfected cells. However, the HSV-1 VPK- mutant had no significant effect on CE accumulation. The relationship between VPK activity and these alterations in cholesterol metabolism was further supported by the observation that staurosporine and calphostin C (protein kinase inhibitors) reduced protein kinase activity in HSV-1-infected cells. These results suggest several potential mechanisms by which alterations in kinase activities in response to HSV-1 infection of vascular cells may alter cholesterol trafficking processes that eventually lead to CE accumulation.

Arteries↗
PubMed2002

Antibody-mediated control of persistent gamma-herpesvirus infection.

The human gamma-herpesviruses, EBV and Kaposi's sarcoma-associated herpesvirus, establish life-long latency and can reactivate in immunocompromised individuals. T cells play an important role in controlling persistent EBV infection, whereas a role for humoral immunity is less clear. The murine gamma-herpesvirus-68 has biological and structural similarities to the human gamma-herpesviruses, and provides an important in vivo experimental model for dissecting mechanisms of immune control. In the current studies, CD28(-/-) mice were used to address the role of Abs in control of persistent murine gamma-herpesvirus-68 infection. Lytic infection was controlled in the lungs of CD28(-/-) mice, and latency was maintained in B cells at normal frequencies. Although class-switched virus-specific Abs were initially generated in the absence of germinal centers, titers and viral neutralizing activity rapidly waned. T cell depletion in CD28(-/-) mice with compromised Ab responses, but not in control mice with intact Ab responses, resulted in significant recrudescence from latency, both in the spleen and the lung. Recrudescence could be prevented by passive transfer of immune serum. These data directly demonstrate an important contribution of humoral immunity to control of gamma-herpesvirus latency, and have significant implications for clinical intervention.

Animals↗
PubMed2002

Prophylaxis of herpesvirus infections in immunocompetent and immunocompromised older patients.

In older patients, prophylaxis of herpesvirus infections mainly involves preventing the recurrence of herpes simplex virus (HSV) and complications of herpes zoster in immunocompetent patients, while in immunocompromised patients it is more concerned with the prevention of opportunistic virus reactivation. HSV ocular infection is the most frequent cause of corneal blindness in the US. The effectiveness of aciclovir 400mg twice daily in preventing the recurrence of HSV eye disease in immunocompetent patients has been well demonstrated. The issue of treatment duration for patients with highly recurrent ocular herpes remains unresolved. Post-herpetic neuralgia (PHN) is one of the most common neuralgic illnesses worldwide. Some progress in prevention of PHN has been made with a combination of antiviral therapy (famciclovir or valaciclovir), started within 72 hours of onset of the rash, and analgesic treatment. However, the best prevention of PHN is the prevention of herpes zoster disease, and the varicella vaccine is an option which over the next few years will be tested in clinical trials. For immunocompromised patients of any age, restoring immunity prevents herpesvirus disease, as demonstrated for cytomegalovirus (CMV) in AIDS patients receiving highly active antiretroviral therapy. Specific antiviral therapy during the initial period after transplantation could prevent reactivation of HSV or CMV in seropositive recipients. Whether pre-emptive therapy or prophylaxis with ganciclovir is the optimal approach against CMV remains controversial, and the relative merits and limitations of each approach may guide the choice. In stem cell transplantation, pre-emptive therapy with foscarnet avoids the neutropenia and related complications associated with ganciclovir. In renal transplant recipients, universal prophylaxis of CMV infection with valaciclovir has the same efficacy as ganciclovir. Although it is relatively toxic, cidofovir should be further evaluated because of its in vitro activity against most DNA viruses.

Aged↗
PubMed1999

Human herpesvirus 8 (Kaposi's sarcoma-associated herpesvirus) infection in men receiving treatment for HIV-1 infection.

OBJECTIVE: To determine the prevalence of human herpesvirus 8 (HHV-8) infection in men treated for HIV-1 infection in Denver, Colorado. DESIGN: Cross-sectional analysis METHODS: Blood samples were obtained from 216 HIV-1-infected men. Antibody to latency-associated nuclear antigen (LANA) was detected by an immunofluorescent assay and the presence of HHV-8 in peripheral blood mononuclear cells (PBMC) was detected by polymerase chain reaction amplification. RESULTS: Among HIV-1-infected men who did not have Kaposi's sarcoma (KS), prevalence of HHV-8 infection was 46% (95% confidence interval [CI], 0.39-0.52). LANA seropositivity was common both among subjects with KS and subjects without KS (69% versus 42%; p = .06), but detection of HHV-8 DNA in peripheral blood was strongly associated with a diagnosis of KS (44% versus 10%; p = .001). In a univariate analysis of study subjects without KS, neither the odds of LANA seropositivity nor detection of HHV-8 DNA in PBMC was significant for CD4+ lymphocyte count, HIV-1 virus load, the use of three drug antiretroviral regimens or the prior occurrence of non-KS AIDS-related conditions. CONCLUSION: Although antibodies to HHV-8 are common among HIV-1-infected men, detection of HHV-8 DNA in PBMC is uncommon and is associated with a diagnosis of Kaposi's sarcoma.

AIDS-Related Opportunistic Infections↗
PubMed2006

Use of a multiantigen detection algorithm for diagnosis of Kaposi's sarcoma-associated herpesvirus infection.

The ability to readily and accurately diagnose Kaposi's sarcoma-associated herpesvirus (KSHV, or human herpesvirus 8) infection in individuals remains a demanding task. Among the available diagnostic methods, sensitivities and specificities range widely, and many are inadequate for large-scale screening studies. We examined a serological algorithm for detecting KSHV in human sera having high sensitivity and specificity. This method uses previously described open reading frame (ORF) K8.1 and ORF65 peptide-based enzyme-linked immunosorbent assays and a novel purified recombinant full-length LANA1 protein. We generated two multiantigen algorithms: one that maximized sensitivity and one that maximized specificity. These serological algorithms were then used to evaluate seroprevalence rates among populations of clinical and epidemiological importance. The serological algorithms yielded sensitivities of 96% and 93% and specificities of 94% and 98% for the more sensitive and specific algorithms, respectively. Among kidney donors, seroprevalence was low, 4.0% (2/50), and similar to that of blood donors (P = 0.46; odds ratio [OR], 1.4; confidence interval [CI], 0.14 to 7.9) using the highly specific algorithm. Using the sensitive algorithm, 8.0% (4/50) were infected compared to 6.4% (16/250) observed among blood donors (OR, 1.3; CI, 0.41 to 4.0; P = 0.43). Among subjects requiring bone marrow transplantation, seroprevalence rates were not elevated compared to those of blood donors (OR, 2.0; 95% CI, 0.10 to 122.9; P = 0.50). Because the need for high-quality KSHV detection methods are warranted and because questions remain about the optimal methods for assessing KSHV infection in individuals, we propose a systematic approach to standardize and optimize the assessment of KSHV infection rates using a combination of established and novel serological assays and methods.

Algorithms↗
PubMed1980

Inactivated vaccine for parrot herpesvirus infections (Pacheco's disease).

Four tests of an inactivated emulsified vaccine against a herpesvirus infection (Pacheco's disease) in bodgerigars demonstrated that an effective vaccine could be produced with concentrated virus. Virus was propagated in chicken kidney cells, and cells and fluid were harvested 3 to 5 days after inoculation and sonicated. The virus was concentrated 100 x by centrifugation to produce a multiple emulsion vaccine that was protective against IM challenge exposure with live virus. The serologic response after vaccination was negligible, and many survivors to virus challenge exposure did not show a positive titer.

Animals↗
PubMed1991

Herpesvirus infection: an overview of the clinical manifestations.

Herpesviruses include seven human viruses and numerous animal viruses. The human herpesviruses, in addition to their trivial names, are named from 1 to 7. The two most recently discovered herpesviruses thus being Human herpesvirus 6 and 7. Human herpesvirus 6 is the aetiologic agent causing exanthema subitum. Human herpesvirus 7 has, as yet, not been associated with any disease. A characteristic feature of the herpesviruses is the persistence in a latent form after primary infection which may later cause reactivated infection resulting in considerable morbidity, for example, in genital herpes. The clinical spectrum of herpes infections is very broad. In general, the primary infection is more severe than the reactivated. Other important determinants of morbidity are the patients' age and immune status. Many severe herpes infections are almost exclusively seen in immunocompromised patients. This review deals with the clinical manifestations of herpetic infections in normal and immunocompromised hosts with emphasis on the clinical recognition.

Chickenpox↗
PubMed1984

Herpesvirus infection of cornea allografts.

This report describes three patients who have in common an occurrence of ocular epithelial herpes infection following a penetrating keratoplasty for a corneal opacity unrelated to herpesvirus infection. It may be that patients undergoing episodes of graft rejection are at increased risk for the reactivation of herpesvirus latent in the trigeminal ganglia, and corticosteroids should be used with this in mind. Because virtually all adults have been exposed to herpes and therefore harbor latent virus, a viral etiology should be considered for lesions in post-penetrating keratoplasty patients. Although the occurrence of this possibly rejection-related reactivation of herpes simplex virus is undoubtedly rare, management of potential cases of this nature should take this possibility into account.

Adult↗
PubMed2000

Immunological hiding of herpesvirus-infected cells.

Over the past years, numerous research groups have discovered various strategies that herpesviruses use to hide themselves from recognition by the immune system of their hosts. The current review gives a summary of this research, with emphasis on the mechanisms by which herpesvirus-infected cells escape from elimination by complement, phagocytes, cytotoxic T-lymphocytes and/or natural killer cells.

Animals↗
PubMed1999

Feline herpesvirus infection in a group of semi-captive cheetahs.

Clinical disease caused by feline herpesvirus type-1 in wild felid species is similar to that in domestic cats. Herpesviruses are endemic in free-ranging lions in South Africa but actual clinical disease due to them has not been reported in free-ranging felids. The first reports of feline herpesvirus infection associated with clinical disease in wild felids came from Australia and the USA in 1970. Subsequent reports of clinical disease in cheetahs and other wild felid species were limited to captive animals. This report deals with clinical disease in a group of semi-captive cheetahs in which 18 animals were affected, and included 12 adult males, 4 adult females and 2 subadults. No mortalities occurred in this group, the most common clinical signs being sneezing, nasal discharge and loss of appetite.

Acinonyx↗
PubMed1985

Treatment of herpesvirus infections in the immunocompromised host.

Major advances have been made in the treatment of herpesvirus infections in the compromised host. Acyclovir is clearly effective in the treatment of HSV infection, and preferable to vidarabine for this purpose. Additional information about the optimal use of acyclovir for treatment or prophylaxis and about the ultimate significance of the phenomena of acyclovir resistance and possible suppression of the specific immune response are needed. The major challenge at this time is the rapid clinical or virologic diagnosis of HSV infection, especially the rarer manifestations such as HSV pneumonia or encephalitis, so that effective therapy can be initiated. The serious manifestations of VZV infection (e.g. cutaneous and visceral dissemination) can also be controlled with either vidarabine or acyclovir, although definition of the agent of choice is still lacking. More information is needed to define the relative efficacy of acyclovir compared with vidarabine, and also to define better treatment regimens for the prevention of post-herpetic neuralgia which remains a major source of morbidity. Use of either oral or topical acyclovir and anti-inflammatory agents in combined regimens is being studied. Interferon, although effective, has little present role in view of the availability of both acyclovir and vidarabine, although it is of interest as a model of an agent that can be administered to outpatients or used in synergistic regimens. The challenge for treatment of CMV is the development of an agent which is effective in vivo. Several promising agents are on the horizon, but much initial work must be done before their effectiveness will become apparent.(ABSTRACT TRUNCATED AT 250 WORDS)

Acyclovir↗