[Beta-herpesvirus infection of the central nervous system].
Explore the source record for details and available documents.
AIDS-Related Opportunistic Infections↗
SEARCH · Search PubMed
Results for “HERPESVIRUS INFECTIONS”
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Kaposi sarcoma-associated herpesvirus infects monotypic (IgM lambda) but polyclonal naive B cells in Castleman disease and associated lymphoproliferative disorders.
In a previous study, it was shown that the Kaposi sarcoma-associated herpesvirus (KSHV) was specifically associated with monotypic (IgMlambda) plasmablasts in multicentric Castleman disease (MCD). The plasmablasts occur as isolated cells in the mantle zone of B-cell follicles but may form microlymphoma or frank plasmablastic lymphoma. To determine the clonality and cellular origin of the monotypic plasmablasts, the rearranged Ig genes in 13 patients with KSHV-related MCD, including 8 cases with microlymphomas and 2 with frank lymphomas, were studied. To investigate the role of the interleukin 6 (IL-6) receptor signaling in the pathogenesis of MCD and associated lymphoproliferative disorders, viral IL-6 and human IL-6 receptor expression was examined. KSHV-positive plasmablasts were polyclonal in MCD-involved lymphoid tissues in all cases and microlymphomas in 6 of 8 cases. Monoclonal KSHV-positive plasmablasts were seen in microlymphomas of 2 cases and in both frank lymphomas. Despite their mature phenotype, KSHV-positive plasmablasts did not harbor somatic mutations in the rearranged Ig genes, indicating origination from naive B cells. Viral IL-6 was expressed in 10% to 15% of KSHV-positive plasmablasts, whereas the human IL-6 receptor was expressed in most KSHV-positive cells. Thus, KSHV infects monotypic but polyclonal naive B cells and is associated with a range of lymphoproliferative disorders from polyclonal isolated plasmablasts and microlymphomas to monoclonal microlymphoma and frank plasmablastic lymphomas in MCD patients. Activation of the IL-6 receptor signaling pathway may play a role in differentiation of KSHV-infected naive B cells into plasmablasts and development of lymphoproliferative lesions. (Blood. 2001;97:2130-2136)
Antigens, Viral↗
The early pathogenesis of turkey herpesvirus infection in chickens and turkeys.
The early responses of chickens and turkeys to infection with two strains of turkey herpesvirus (FC 126 and a recent field isolate, T-5A) were compared. All birds had similar virus rescue patterns from the spleen, regardless of virus strain used for infection. Productive-restrictive infections as indicated by the presence of viral antigens were found only in the spleens of infected turkeys. Viral antigens were not found in bursa or thymus but were found intermittently and at low levels in the skin. Small focal accumulations of lymphocytic cells were found in the nerves of all groups of birds 7 and 14 days postinoculation.
Animals↗
Altered cholesteryl ester cycle is associated with lipid accumulation in herpesvirus-infected arterial smooth muscle cells.
We describe herein the effects of Marek's disease herpesvirus (MDV) on cholesterol and cholesteryl ester metabolism in cultured chicken arterial smooth muscle cells. Infection of arterial smooth muscle cells from specific pathogen-free chickens with MDV, but not a virus control, herpesvirus of turkeys led to a 7-10-fold increase in the accumulation of free and esterified cholesterol and a 2-fold increase in phospholipids. The cellular lipid changes observed in the MDV-infected arterial smooth muscle cells resulted, in part, from the following: decreased low-density lipoprotein-cholesteryl ester hydrolysis due to decreased lysosomal (acid) cholesteryl ester hydrolytic activity; increased de novo synthesis of cholesterol; decreased excretion of free cholesterol; and, both increased cholesteryl ester synthetic activity and decreased cytoplasmic (neutral) cholesteryl ester hydrolytic activity which resulted in increased incorporation of oleic acid into cholesteryl ester. Other changes noted in the MDV-infected cells as compared to uninfected cells included a 2-fold increase in both total protein synthesis and lysosomal and microsomal marker enzyme activities. These alterations in lipid and protein metabolism in MDV-infected arterial smooth muscle cells may explain in part our in vivo findings that herpesvirus (MDV) infection of specific pathogen-free chickens fed a normocholesterolemic diet will induce arterial thickening and lipid accumulation resembling human atherosclerosis.
Animals↗
Regulation of CD1d expression and function by a herpesvirus infection.
Little is known about the role of CD1d-restricted T cells in antiviral immune responses. Here we show that the lytic replication cycle of the Kaposi sarcoma-associated herpesvirus (KSHV) promotes downregulation of cell-surface CD1d. This is caused by expression of the 2 modulator of immune recognition (MIR) proteins of the virus, each of which promotes the loss of surface CD1d expression following transfection into uninfected cells. Inhibition of CD1d surface expression is due to ubiquitination of the CD1d alpha-chain on a unique lysine residue in its cytoplasmic tail, which triggers endocytosis. Unlike MIR-mediated MHC class I downregulation, however, CD1d downregulation does not appear to include accelerated lysosomal degradation. MIR2-induced downregulation of CD1d results in reduced activation of CD1d-restricted T cells in vitro. KSHV modulation of CD1d expression represents a strategy for viral evasion of innate host immune responses and implicates CD1d-restricted T cells as regulators of this viral infection.
Antigens, CD1↗
Genital herpesvirus infection in women attending a venereal diseases clinic.
Routine cervical viral cultures (and cultures from lesions if present) were performed on 2630 female patients attending a venereal diseases clinic over a period of four years. Of these patients 96 (3.7%) had genital herpetic infection; of these 23 (24%) were asymptomatic. The association of herpesvirus with other genital infections is considered, but no increase in the incidence of Neisseria gonorrhoeae, Trichomonas vaginalis, and genital warts was found; there was an increased incidence of Candida albicans. A significantly higher percentage of the patients with herpesvirus took oral contraceptives. The findings are discussed and compared with previous reports.
Adolescent↗
The differential diagnosis of herpesvirus infections in man and animals.
The precise number of human and nonhuman herpesviruses is unknown. It is recognized, however, that the complex antigenic components of this group of viruses and their group interrelationships make specific differentiation of certain herpesviruses extremely difficult with routine serologic procedures. The question of differentiating herpes simplex (H. hominis) infection from B virus (H. simiae) infection frequently requires resolution. When SA8, another primate herpesvirus (principally of African primates) is also involved, differentiation becomes more difficult. The serum neutralization (SN) test, currently the procedure of choice for serologic diagnosis, is not without error. A number of factors control its specificity and variability. Neither EIA, RIA nor FA improves the specificity. Polyarcylamide electrophoresis of the highly lethal B virus indicates the presence of antigens (polypeptides and glycoproteins) distinct from those in other herpesviruses, which may aid in the specific diagnosis, particularly when these antigens are used for the production of monoclonal antibody. DNA fragments have been identified in B virus by restriction endonuclease analysis that appear to be unique for this agent in comparison to human herpesviruses types 1 and 2.
Animals↗
Transmission and scanning electron microscopy of experimental pulmonary simian varicella (Delta herpesvirus) infection in African green monkeys (Cercopithecus aethiops).
The lungs of African green monkeys infected with simian varicella virus (Delta herpesvirus) were examined by scanning and transmission electron microscopy. Endothelial cell shrinkage, oedema formation and necrosis characterized the scanning electron microscopy of the affected vasculature. Oedema of the interalveolar septa with swelling of the capillary endothelial cells was observed by transmission electron microscopy. Numerous viral particles were associated with a generalized area of necrosis of the alveolar wall.
Animals↗
Relation between common antigen and membrane antigens associated with Marek's disease herpesvirus and turkey herpesvirus infections.
The appearance of two kinds of membrane antigen (MA) in Marek's disease herpesvirus (MDHV) or herpesvirus of turkey (HVT) infected cells was examined using antiserum to the common antigen (common-Ag). No early-appearing MA(EMA) was detected in these cultures until 16 hours post-inoculation, after which a number of cells in these cultures had late-appearing membrane antigen (LMA) as detected by immunofluorescence (IF). Fluids from cultures infected with these viruses were examined for the presence of the common-Ag by agar-gel precipitation (AGP) test. No common-Ag was detected until 16 hours, but after 24 hours, it was detected by AGP test. These results suggest that the common-Ag is related to LMA but not to EMA.
Animals↗
RNA synthesis in cells infected with herpes simplex virus: analysis of high molecular weight and symmetrical viral transcripts in herpesvirus infected cells.
Explore the source record for details and available documents.
Base Sequence↗
Epidemiology of Epstein-Barr virus, cytomegalovirus, and Kaposi's sarcoma-associated herpesvirus infections in peripheral blood leukocytes revealed by a multiplex PCR assay.
A multiplex polymerase chain reaction (PCR) has been developed for the simultaneous detection of Epstein-Barr virus (EBV), cytomegalovirus (CMV), and Kaposi's sarcoma-associated herpesvirus (KSHV) in a clinical sample. Primers of multiplex PCR were designed to amplify specific regions of the EBV EBNA1, CMV IE2, and KSHV LANA genes. This multiplex PCR assay was found to have detection sensitivities of 1-10 copies of purified viral DNA cloned into the plasmid. To assess diagnostic and pre-clinical applications with this method, we utilized KSHV-positive primary effusion lymphoma (PEL) cells, EBV-positive Burkitt's lymphoma cells, CMV-infected fibroblast cells, and clinically prepared peripheral blood leukocytes (PBLs) that had been infected with viruses. We found that this multiplex PCR assay has high sensitivity and specificity for simultaneous detection of EBV, CMV, and KSHV genomes in a single amplification from a clinical material. Using this multiplex PCR assay, we investigated the prevalence of EBV, CMV, and KSHV in PBL samples from normal Japanese randomly selected. KSHV, EBV, and CMV genomes were detected in samples from 2 (0.2%), 377 (39.5%), and 27 (2.8%) of the 953 blood donors, respectively. Interestingly, both EBV and CMV genomes were detected in samples from all KSHV-positive donors.
Blood Donors↗
[Importance of molecular biology in retrovirus and herpesvirus infections].
Molecular biology has long been used as a tool for basic research in virology. Its medical use is recent and has been supported both by numerous technical improvements and the discovery of new human viruses. This is illustrated by the emergence of human immunodeficiency virus (HIV)-1, HIV-2, human T-cell leukemia virus (HTLV)-I/II, and human herpesviruses (HHV) 6, 7 and 8. Polymerase chain reaction (PCR) gave a major boost to an extended use of molecular biology techniques. This resulted in a better knowledge of human viral infections as illustrated by studies on HIV and HHV-8. New viruses have been characterized. Molecular markers have permitted analysis of virus transmission cases, classification of genetic variants and detection of mixed infections. The quantitation of viral load has led to a better understanding of chronic infections and reactivations. As a tool for diagnosis, molecular biology is not yet considered as a universal alternative to classical procedures such as serology and antigen detection. However, major improvements in molecular biology techniques might question current diagnosis strategies in the very near future.
HIV↗
Herpesvirus infections in xenotransplantation: pathogenesis and approaches.
Infectious risk remains an important consideration in the clinical application of xenotransplantation. Vascularized xenografts create unique immunological niches in which bidirectional transmission of pathogens between donor and recipient may occur. Enhanced replication of many pathogens is stimulated by the immune responses induced by transplantation and by the immune suppression used to prevent graft rejection. Herpesviruses are the prototype viruses that are activated during immunosuppression. Quantitative diagnostic molecular assays have been developed for the known herpesviruses causing infection in pigs. Recent data suggest that some herpesviral infections, such as porcine cytomegalovirus, may be excluded from swine used as source animals by careful breeding, while others will require novel strategies for control. This review focuses on porcine and baboon herpesviruses in pig-to-non-human primate solid organ xenotransplantation including direct effects (tissue damage), indirect effects (coagulopathy, rejection), and possible approaches to these infections.
Animals↗
Experimental feline herpesvirus infection in the pregnant cat.
Intravenous inoculation of pregnant cats with feline herpesvirus produced minimal illness but resulted in abortion, intrauterine fetal death and congenital fetal infection. Placental lesions included multiple infarcts in the placental labyrinth, thrombosis of maternal vessels in the endometrium and placenta, and multifocal necrosis of the giant-cell trophoblast and endometrial epithelium in the junctional zone of the placenta associated with eosinophilic intranuclear inclusion bodies. The virus was isolated from all the placentas and uteri but from none of the fetuses aborted 6-9 days after maternal intravenous inoculation. Viral antigen was demonstrated in the uterine vessels and in the junctional zone of the placenta at this time. On postinoculation day 26, viral antigen was demonstrated in the chorioallantoic membrane on the fetal side of the placenta and in the liver of a congenitally infected fetus. Although all 4 pregnant cats inoculated intranasally with feline herpesvirus aborted, neither virus, viral antigen nor significant lesions were detected in the uteri, placentas or fetuses. Abortion after intranasal inoculation was interpreted as a nonspecific reaction secondary to the severe, debilitating upper respiratory disease that occurred.
Abortion, Spontaneous↗
Epstein-Barr virus and other herpesvirus infections in Kawasaki syndrome.
Epstein-Barr virus (EBV), a possible cause of Kawasaki syndrome (KS), is not pathenogenically associated with KS in Hawaii. The prevalence of EBV capsid antibody in KS patients was found not to differ significantly from that in controls, and the antibody response in those infected with EBV was the same as that in other children similarly infected. No EBV was isolated from acute-phase patients. All patients with capsid antibody at the onset of KS also had Epstein-Barr nuclear antigen antibody: 36 patients developed antibody within 3 months after onset of KS; in 10, EBV infection could have been coincidental with the disease. Cytomegalovirus (CMV) was isolated from 9 patients with KS and 10 controls. A similar number of controls and patients had antibody to human herpesvirus 6 (HHV6); one patient seroconverted. None of the herpes viruses (EBV, CMV, HHV6, varicella-zoster virus, or herpes simplex virus) plays a unique or dominant role in the etiology or pathogenesis of KS in Hawaii.
Age Factors↗
Latent murine gamma-herpesvirus infection is established in activated B cells, dendritic cells, and macrophages.
Intranasal infection of mice with the murine gamma-herpesvirus MHV-68 results in an acute lytic infection in the lung, followed by the establishment of lifelong latency. Development of an infectious mononucleosis-like syndrome correlates with the establishment of latency and is characterized by splenomegaly and the appearance of activated CD8+ T cells in the peripheral blood. Interestingly, a large population of activated CD8+ T cells in the peripheral blood expresses the V beta 4+ element in their TCR. In this report we show that MHV-68 latency in the spleen after intranasal infection is harbored in three APC types: B cells, macrophages, and dendritic cells. Surprisingly, since latency has not previously been described in dendritic cells, these cells harbored the highest frequency of latent virus. Among B cells, latency was preferentially associated with activated B cells expressing the phenotype of germinal center B cells, thus formally linking the previously reported association of latency gene expression and germinal centers to germinal center B cells. Germinal center formation, however, was not required for the establishment of latency. Significantly, although three cell types were latently infected, the ability to stimulate V beta 4+CD8+ T cell hybridomas was limited to latently infected, activated B cells.
Animals↗
Induction of chemokine production by latent Kaposi's sarcoma-associated herpesvirus infection of endothelial cells.
Infection with Kaposi's sarcoma (KS)-associated herpesvirus (KSHV) is linked strongly to development of KS, an endothelial neoplasm also characterized by striking neoangiogenesis and infiltration with inflammatory cells. To elucidate the links between endothelial infection and inflammation, primary human umbilical vein endothelial cells (HUVECs) were examined for the production of chemokines following latent KSHV infection. Several chemokines that are produced in the ground state, including MCP-1, NAP 2 and RANTES, are upregulated significantly by KSHV infection. Moreover, the chemokine CXCL16, which is nearly absent in uninfected cells, is induced significantly following infection. This induction is attributable primarily to expression of vFLIP, a known inducer of NF-kappaB. CXCL16 induces the chemotaxis of activated T cells, whose products have been proposed to positively regulate KS tumour-cell survival and growth. Whilst CXCL16 has also been proposed as a direct endothelial chemoattractant and mitogen, neither proliferation nor chemotaxis of HUVECs was observed following CXCL16 exposure. These results suggest that CXCL16 induction by KSHV contributes to the inflammatory phenotype of KS, but plays little role in the recruitment of endothelial spindle cells.
Cells, Cultured↗
Parma wallaby herpesvirus infection.
Three Parma wallabies (Macropus parma) were inoculated with a herpesvirus recovered from a captive Parma wallaby with fatal naturally-occurring disease. Two intravenously inoculated animals died after 5 days and one animal infected via the conjunctiva and nasal mucosa was killed when moribund at 7 days. An additional two wallabies held in contact with the others became infected; they were killed at 11 days, when one was severely affected and one was mildly affected. All had small vesicles and ulcers of the skin of the upper and lower lips, eyelids, anogenital area and adjacent genital mucosa. Small vesicles and ulcers and large ulcers, with adherent necrotic epithelium and inflammatory debris, were present on the mucosa of the upper lips and adjacent gums and the conjunctiva. Numerous large basophilic or eosinophilic intranuclear inclusion bodies were observed in the epithelial cells of these vesicles and ulcers and of adjacent hair follicles and sebaceous glands. There was a mild to moderately severe rhinitis. Keratitis was present in two wallabies. Liver lesions were present in two animals but were unlike those seen in herpesviral hepatitis in other species.
Animals↗