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At least 109 records · Page 6Linked to original sources
PubMed1987

[Pediatric kidney transplants and herpesvirus infections].

Twenty seven children were followed up prospectively after renal transplant for evidence of infection and illness due to cytomegalovirus (CMV), Epstein-Barr virus (EBV) and varicella zoster virus (VZV). Virus shedding and serological status were tested at transplant day, biweekly for two months, monthly for six months and trimestrialy thereafter. Determinations were done by complement fixation test. CMV isolation was established by microscopic examination of urinary cultures. Primary infections were objetivated in 27 cases (18 CMV, 1 EBV, 8 VZV) and reinfection in 3 (2 CMV, 1 VZV). Irreversible allograft rejection related to infection was disclosed in 2 patients (1 primary CMV infection, 1 VZV reinfection). Renal function impairment occurred only with CMV (6 primary and 1 secondary infections). One patient died with CMV over infection.

Child↗
PubMed1985

Herpesvirus infections in the immunocompromised patient.

The herpes group viral infections in the T cell immunocompromised host may be seen as a disturbance of a delicate balance between the host and well adapted commensals. The clinical aspect of this disturbance is highly variable but may cause the destruction of the host due to widespread organ damage or prolonged debilitating illnesses. An important aspect is the immunosuppressive effect of the infections themselves leading to a number of superinfections, often with unusual pathogens, difficult to treat. Further problems arise from the potential onchogenic effect of some of these viruses such as EBV induced lymphomas. On the threshold to the era of effective antiviral chemotherapy, two major problems are still present: identification of the precise immunological mechanisms controlling the latency/reactivation of the different viruses and the establishment of reliable methods for rapid diagnosis, crucial for the treatment of patients with atypical clinical presentation and atypical serological responses.

Antibodies, Viral↗
PubMed1983

Recurrent polyneuropathy with multiple herpesvirus infections.

A 4-year-old boy developed typical acute polyneuritis at 2 years of age and returned to fully normal status in 2 months. When he was 4 years old, an identical neurologic syndrome recurred at the same time that his sister was determined to have classic infectious mononucleosis. Both siblings then had positive Monospot tests. The boy with recurrent symmetrical neuropathy had an initial Epstein-Barr virus-viral capsid antibody (EBV-VCA) serum titer of 1:160 and this dropped to 1:40 after 1 month. A persistent complement fixation titer to cytomegalovirus (CMV) of 1:64 was measured in his serum and his concentrated CSF contained a CMV complement fixation antibody titer of 1:32, a rare finding in an age-matched control group. Cultures of his urine, buffy coat, and saliva for CMV were negative. Electrophoresis of his CSF revealed oligoclonal bands, several of which were also present in his serum. It seems most likely, but not proven, that the clinical paralysis was caused initially by a CMV infection and that the Epstein-Barr virus infection reactivated the latent CMV to produce the recurrent weakness.

Antibodies, Viral↗
PubMed1993

[Recent information about the etiopathogenesis of paretic-paralytic forms of herpesvirus infection in horses].

From spring 1990 to summer 1991 we investigated 21 horses with clinical symptoms of EHV-infection by means of serological and virological methods including DNA-hybridization to identify the causative agents. The results indicated that, as already reported by us, EHV4 may also cause the paralytic form of the infection. The possibility of double infection with EHV4 and EHV1 cannot be excluded. In 3 out of 21 affected horses we could investigate brain tissue and/or spinal fluid by Dotblot hybridization with EHV1 and EHV4-DNA. The investigated samples of all three horses showed hybridization with EHV4-DNA, without or with less pronounced reaction with EHV1-DNA. The results were confirmed by serological investigation. Brain tissue and cerebrospinal fluid from two horses with paretic or paralytic disorders (1979 and 1980) was also investigated by DNA hybridization. In the liquor of one horse--a 5-month-old foal with neonatal ataxia--we detected EHV1-DNA. The other horse showed a strong reaction with EHV1 and a weaker reaction with EHV4 in its brain material and no hybridisation in the cerebrospinal fluid. The results are discussed.

Animals↗
PubMed1996

Herpesvirus infections.

There are presently seven known herpes viruses that infect humans. Those viruses are important in the fields of oral medicine and dentistry because they cause oral lesions, infect saliva, and cause serious and potentially life-threatening infections in patients whose immune systems are compromised by cancer chemotherapy, immunosuppressive drugs, or HIV infection. This article reviews the basic virology and clinical manifestations of the herpes viruses while highlighting the clinical aspects of herpes-related diseases important to dentistry.

Chickenpox↗
PubMed1996

Factors that influence activated CD8+ T-cell apoptosis in patients with acute herpesvirus infections: loss of costimulatory molecules CD28, CD5 and CD6 but relative maintenance of Bax and Bcl-X expression.

The expanded CD8+ T-lymphocyte population arising in response to viral infection controls the virus but could also prove damaging to the host unless safely removed at the end of the immune response. Apoptosis provides a mechanism whereby this can be achieved, as apoptotic cells are recognized and engulfed by macrophages. Peripheral blood CD8+ T lymphocytes from individuals with acute viral infections were highly susceptible to apoptosis after short-term culture in vitro. This spontaneous cell death could be prevented by interleukin-2 (IL-2) and was related to a decreased expression of Bcl-2 but not Bax or Bcl-XL, additional molecules that promote or prevent apoptosis, respectively, as well as an increase in CD95. After stimulation with anti-CD3 antibody, T cells from these patients also underwent an activation-induced cell death (AICD) that could not be prevented by IL-2. Interestingly, CD8+ T cells from this patient group expressed lower than normal levels of three costimulatory molecules, CD28, CD5 and CD6, suggesting that stimulation in the absence of a second signal is a possible mechanism for the defective reactivation of these cells. Thus multiple mechanisms, including loss of Bcl-2, increased CD95 and loss of costimulatory molecules, place constraints on the survival and reactivation of activated CD8+ T cells after viral infections. This enables immune activation to be controlled and cellular homeostasis to be re-established during resolution of viral diseases in vivo.

Acute Disease↗