Kaposi's sarcoma-associated herpesvirus infection and multiple myeloma.
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Antibodies, Viral↗
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Results for “HERPESVIRUS INFECTIONS”
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Kaposi's sarcoma-associated herpesvirus infection and multiple myeloma.
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Antibodies, Viral↗
Kaposi's sarcoma-associated herpesvirus infection and multiple myeloma.
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Antibodies, Viral↗
[Kaposi sarcoma-associated Herpesvirus infection of dendritic cells in bone marrow in patients with myelomatosis].
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Bone Marrow↗
Glial cell responses to herpesvirus infections: role in defense and immunopathogenesis.
Glial cells can respond to herpesvirus infections through the production of cytokines and chemokines. Although specific interactions between resident glia and lymphocytes that infiltrate the infected brain remain to be defined, the presence of T cell chemotactic signals in microglial cell supernatants following infection with cytomegalovirus or herpes simplex virus has led to the concept that chemokines initiate a cascade of neuroimmune responses that result in defense of the brain against herpesviruses. While chemokines may play a defensive role by attracting T cells into the brain, aberrant accumulation of lymphocytes may also induce brain damage. Host defense mechanisms must balance control of herpesvirus spread with associated undesirable immunopathologic effects. A growing body of evidence suggests that through complex networks of chemokines and cytokines produced in response to herpesvirus infection, glial cells orchestrate a cascade of events that result in successful defense of or damage to the brain.
Animals↗
[Prevention and therapy of herpesvirus infections].
The group of the human-pathogenic herpesviruses comprises five subgroups: Herpes simplex virus type 1 (HSV-1), Herpes simplex virus type 2 (HSV-2), varicella zoster virus (VZV), cytomegalovirus (CMV), and Epstein-Barr virus (EBV). Primary infection with these ubiquitous herpesviruses usually occurs in childhood or during adolescence and frequently remains inapparent. However, it can also give rise to a variety of clinical pictures. Important clinical manifestations of herpesvirus infections are mucocutaneous lesions (HSV-1, HSV-2, VZV) self-limited, lymphoproliferative diseases (CMV, EBV) and congenital malformations (CMV). Primary infection with herpesviruses leads to a persistent infection of the host. This clinically silent condition of latency can be interrupted and may cause pathological symptoms to recur by reactivation of latent herpesviruses. A classical example of the clinical manifestation of herpesvirus reactivation is herpes zoster following an overcome varicella disease. The mechanism of herpesvirus reactivation has not yet been fully clarified. Reactivation of herpesviruses might be attributable to a weakening of the cellular immunodefence. For the control of viral infections mainly two cellular effector systems are responsible: unspecific, cytotoxic, natural killer (NK) cells and specific cytotoxic thymus-dependent (T) lymphocytes. The functional impairment of these cytotoxic active cells my cause herpesvirus reactivation in immunodeficient or immunosuppressed persons. Interference with the immunological control function may also contribute to the genesis of herpesvirus-associated tumours. Such an association between herpesviruses and human tumours is assumed to exist especially in the case of EBV. The frequently life-endangering severity of local or disseminated herpesvirus infections calls for suitable measures ensuring efficient prophylaxis and therapy. However, the possibilities of a specific immunoprophylaxis (vaccine, special immunoglobulins) against herpesvirus infections are still rather limited. The development of antiviral substances has greatly benefited from the introduction of new agents (Acyclovir) and the production of sufficient quantities of interferon (IFN) preparations during the last few years. Impressive results were obtained with the nucleoside-related substance Acyclovir in the prevention and therapy of primary or reactivated HSV-1 or HSV-2 infections. The use of Acyclovir as prophylactic agent produced the effect that recipients of bone-marrow transplants were no longer afflicted by HSV-1 infections.(ABSTRACT TRUNCATED AT 400 WORDS)
Acyclovir↗
Efficacy of acyclovir against herpesvirus infection in Quaker parakeets.
We evaluated the efficacy of acyclovir against experimentally induced herpesvirus infection (Pacheco's parrot disease) in Quaker parakeets. Thirty-two of 40 birds were challenge-exposed with 0.1 ml of a suspension of herpesvirus (10(4) median cell culture infective doses [CCID50]) given IM. Treatment with acyclovir was started 24 hours later and was continued for 7 days. The birds were allotted to 5 groups of 8 birds each. There was a considerable difference in mortality between groups 1-5. Of 8 bird in each group, 6 died in group 1 (control), 1 died in group 2 (gavage), 3 died in group 3 (low dose, IM), 4 died in group 4 (high dose, IM), and none died in group 5 (contact controls). There was a significant (P = 0.023) difference in mortality between groups 1 and 2, thus the oral form of acyclovir administered by gavage was the most efficacious therapeutic regimen. Clinical signs and death occurred after discontinuation of acyclovir in groups 2 and 3, whereas the mean time of death for the control group was 6 days after challenge exposure. Herpesvirus was recovered by inoculation of chick embryo cell culture with pooled tissue suspensions from all birds that died. Histologic evidence of herpesvirus infection was found in most birds that died, with the control group having the most severe lesions. Surviving Quaker parakeets were transferred to cages with seronegative Quaker parakeets with no known exposure to herpesvirus. There have been no deaths attributable to herpesvirus infection in a period exceeding 2 years.
Acyclovir↗
Herpesvirus infection accelerates atherosclerosis in the apolipoprotein E-deficient mouse.
BACKGROUND: Human herpesviruses have been implicated but not proven to be involved in the etiology of atherosclerosis. To determine whether there is a causal relationship, the effect of herpesvirus infection on the development of atherosclerosis was assessed in the apolipoprotein E-deficient (apoE-/-) mouse. METHODS AND RESULTS: In the present study, 3- to 4-week-old apoE-/- mice were infected with murine gamma-herpesvirus-68 (MHV-68). Atheroma formation was accelerated over a 24-week period in infected apoE-/- mice compared with control uninfected apoE-/- mice. Acceleration of atherosclerosis was reduced by antiviral drug administration. Histological analysis of the atheromatous plaques showed no difference between lesions of infected and control mice. Viral mRNA was present in the aortas of infected mice before lesion development on day 5 after infection. This suggests that the virus may initiate endothelial injury, which is believed to be an early event in the development of atherosclerosis. Therefore, the virus may play a direct role in atherosclerosis rather than be an "innocent bystander." CONCLUSIONS: These data demonstrate that a gamma-herpesvirus can accelerate atherosclerosis in the apoE-/- mouse. This study provides the first report of a murine model in which to study the causative role of herpesvirus infection in the development of atherosclerosis.
Animals↗
Skin manifestations of herpesvirus infections.
Currently there are eight human herpesviruses identified that cause disease in both adults and children. Although the manifestations of disease differ with each herpesvirus, cutaneous presentations are common among almost all of them. These skin manifestations may be visually similar among several of these viruses, occasionally making it challenging to diagnose the patient's illness. Laboratory diagnostic testing is commercially available for most of these viruses. Because many herpesvirus infections are self-limiting in immunocompetent hosts, patients require only supportive care. Effective antiviral therapy is available for the more severe cases of infection caused by herpes simplex virus (HSV), varicella zoster virus (VZV), or cytomegalovirus (CMV). Healthcare practitioners should become familiar with the different cutaneous manifestations these viruses may exhibit.
Journal Article↗
Herpesvirus infection of the liver.
The human herpesviruses can produce a wide variety of disease in the liver (Table 7). The immunocompromised host is particularly susceptible to hepatic manifestations of herpesvirus disease. CMV is the most common opportunistic pathogen in the immunocompromised patient. The clinical presentation of hepatic herpesvirus infection is often nonspecific. A high index of suspicion and rapid progression to liver biopsy to document viral replication (alpha- and betaherpesviruses) or outgrowth of virus-infected cells (gammaherpesviruses) can lead to lifesaving therapeutic interventions.
Animals↗
Management of herpesvirus infections in the healthy host.
Human herpesvirus infections continue to be a concern in immunocompetent as well as immunocompromised hosts. They are often life threatening in the immunocompromised patient. In the healthy immunocompetent person the infections tend to be self-limited, although they can directly or indirectly cause periods of severe discomfort and disability, and their treatment can affect productivity, as shown by cost-outcome models. Treatment of primary or secondary episodes in the immunocompetent host is therefore directed toward more rapid resolution of initial and recurrent episodes, thereby limiting the impact of the infections.
Acyclovir↗
Herpesvirus infections in seals: a summary of present knowledge.
This review summarises the occurrence of herpesvirus infections in pinnipeds and data from investigations carried out by the authors. These data demonstrate that herpesvirus isolates collected from harbour seals (Phoca vitulina Linnaeus, 1758) during the 1988 seal epidemic were almost indistinguishable from feline herpesvirus 1 and that Antarctic Weddell's seals (Leptonychotes weddelli Lesson, 1826) carry antibodies against seal herpesvirus from the north-western Europe seal epidemic. The significance of herpesvirus infections in seals is discussed.
Animals↗
Overview of immunopathology of chronic active herpesvirus infection.
Chronic latent infection with human herpesvirus is common; antibody prevalence in the general population varies from 40 to above 95%, for herpesvirus-6 at about 20%. Reactivation occurs in 5-20% of healthy persons. If reactivation coincides with impaired host response, chronic active infection may ensue. Chronic active infection by certain members of the Herpesviridae such as EBV, CMV and HHV-6 is prone to being complicated by autoimmune diseases and atypical lymphoproliferation. Its diagnosis is occasionally rendered difficult by a variety of immunologic interference factors, thus final evaluation must result from clinical, immunopathological and virological cooperation.
Antibodies, Viral↗
Vidarabine therapy for severe herpesvirus infections. An unusual syndrome of chronic varicella and transient immunologic deficiency.
Six patients with severe herpesvirus infections were successfully treated with vidarabine. One patient had a previously undescribed syndrome of chronic cutaneous varicella infection of eight months' duration, associated with transient but complete duppression of lymphocyte response to conconavalin A. Other diagnoses were severe varicella pneumonia, progressive cytomegalovirus pneumonia associated with acute lymphocytic leukemia, herpes simplex encephalitis, severe zoster associated with stage IV lymphoma, and disseminated herpes simplex in a patient receiving high doses of steroids. All patients showed cessation of new lesions or abrupt clinical improvement between days 2 and 4 after initiation of therapy, and all were cured of their clinical infection. Dramatic improvement in all of our patients and the minimal toxicity observed make vidarabine suitable for use in severe herpesvirus infections.
Adolescent↗
[Herpesvirus infections--indications for chemotherapy in dermato-venereology].
Specific antivirals like acyclovir have ameliorated the outcome of severe herpesvirus infections, especially in immunocompromised patients. Varicella can be prevented in high-risk patients after exposure by therapy with varicella-zoster immunoglobulin. Despite this favorable development, there are many unresolved problems in the management of herpesvirus infections, such as the use of acyclovir during pregnancy, the treatment of both motoric neuropathy and postherpetic neuralgia. Chemotherapy-resistant herpesvirus may cause severe syndromes in patients suffering from HIV infection or from iatrogenic immunosuppression. Isolation of resistant viruses provides the stimulus to establish tests of viral resistance and to use antiviral drugs more carefully.
Acyclovir↗
Treatment of cats with ocular disease attributable to herpesvirus infection: 17 cases (1983-1993).
Medical records of 17 cats with ocular disease attributable to herpesvirus injection were reviewed. Herpesvirus infection was confirmed by a positive result on an immunofluorescent antibody test or by detection of dendritic corneal ulcers. Cats were 3 months to 23 years old (mean, 4.8 years). Sex or breed predilections were not evident. Vaccination history was available for 13 cats, 9 of which had been adequately vaccinated against feline viral rhinotracheitis, calici, and panleukopenia viruses. Six cats had a history of respiratory tract disease. Twelve cats were tested for FeLV, and 3 had positive results; 7 cats were tested for feline immunodeficiency virus, with 1 positive result. The most common ocular abnormality seen was conjunctivitis (13/17 cats), followed by dendritic corneal ulcers (10/17 cats). Keratitis was detected in 6 of 17 cats, and nondendritic corneal ulcers in 3 of 17 cats. Corneal sequestra were evident on initial examination or developed during the follow-up period in 4 of 17 cats. Keratoconjunctivitis sicca was diagnosed in 2 of 17 cats, and anterior uveitis was evident in 1 of 17 cats. All cats had 2 or more clinical ocular abnormalities associated with herpesvirus infection. Treatment with topically applied antiviral medications was instituted in 14 cats, including idoxuridine in 7, vidarabine in 4, and trifluridine in 3. Antibiotics were used topically in 10 cats, and atropine was used in 3 cats. Topical administration of corticosteroids was used in 2 cats. Recombinant human alpha-interferon was given orally to 3 cats in conjunction with topical administration of antiviral agents. In addition to medical treatment, 4 cats were treated surgically.(ABSTRACT TRUNCATED AT 250 WORDS)
Administration, Topical↗
[Herpesvirus infections in children with acute lymphatic leukemia].
33 children with acute lymphatic leukemia and 33 healthy controls were longitudinally studied for herpesvirus infections. Active herpes simplex-virus, varicella-zoster virus and cytomegalovirus (CMV) infections were more frequent in patients than in controls. CMV and Epstein-Barr virus infections were often inapparent or associated with infections of the upper respiratory tract. Analysis of serological datas revealed a coincidence of active CVM infection and lethal course of the leukemia. This may be a result of the immunodeficiency in leukemia patients caused by disease and therapy. An additional influence of the immunosuppressive effect of active CMV infections on the course of the disease is discussed.
Adolescent↗
Effect of water temperature on a herpesvirus infection of sea turtles.
The role of water temperature in the induction and maintenance of a dermal herpesvirus infection (gray-patch disease) of young, green sea turtles (Chelonia mydas) was studied under carefully controlled experimental conditions, in which the influence of other recognized stress factors was negligible. A nimals that were subjected to a gradual temperature increase from 25 to 30 degrees C, with subsequent maintenance at 30 degrees C, and those that were abruptly shifted from water at 25 degrees C to water at 30 degrees C showed a significantly shorter period before the onset of clinical signs and an increase in the severity of the lesions when compared with control animals. Animals that were subjected to a gradual increase in water temperature from 25 to 30 degrees C and a subsequent decrease to 25 degrees C, where they were maintained, had a period before onset of clinical signs and severity closer to that of control animals. Our findings indicate that both the induction of clinical gray-patch disease and the severity of the lesions are affected by water temperature and suggest that one possible means of control of this herpesvirus infection under intensive aquaculture conditions might be water temperature manipulation.
Animals↗