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At least 19 recordsLinked to original sources
PubMed1995

Guidelines for the prevention and treatment of B-virus infections in exposed persons. The B virus Working Group.

Cercopithecine herpesvirus 1 (B virus), enzootic among monkeys of the genus Macaca, causes minimal morbidity in its natural host. In contrast, human B-virus infection presents as rapidly ascending encephalomyelitis with a fatality rate of approximately 70%. This infection remains an uncommon result of macaque-related injuries, although the increase in the use of macaques for research on simian retrovirus infection and hepatitis has expanded the number of opportunities for human exposure. In response to this situation, Emory University and the Centers for Disease Control and Prevention jointly sponsored a B Virus Working Group to formulate a rational approach to the detection and management of human B-virus infection. The resulting guidelines are presented herein and are based upon information from published cases, unpublished cases managed by working-group members, knowledge of the behavior of herpes simplex virus, and--in the absence of hard data--the collective judgment of the group. Although consensus among the co-authors existed on the major points covered by these guidelines, opinions varied widely regarding specific recommendations.

Animals↗
PubMed1996

Lamivudine in children with human immunodeficiency virus infection: a phase I/II study. The National Cancer Institute Pediatric Branch-Human Immunodeficiency Virus Working Group.

The safety, tolerability, pharmacokinetic profile, and preliminary activity of lamivudine (2'-deoxy-3'-thiacytidine), a novel cytidine nucleoside analogue with antiretroviral activity, in human immunodeficiency virus (HIV)-infected children beyond the neonatal period were studied. Ninety children received dosages of 1-20 mg/kg/day. Pharmacokinetic evaluation demonstrated serum and cerebrospinal fluid concentrations that increased proportionally to dose. As of January 1994, 11 children had been withdrawn from study for disease progression and 10 because of possible lamivudine-related toxicity, and 6 had died. CD4 and CD8 cell counts remained stable over 24 weeks in therapy-naive children and decrease slightly in previously treated children. Quantitative immune complex-dissociated p24 antigen and HIV RNA were decreased significantly at 12 and 24 weeks. In vitro resistance to lamivudine was documented in sequential virus isolates from some patients by 12 weeks. Lamivudine was well-tolerated and exhibited virologic activity in children, although future use in children is likely to be in combination antiretroviral regimens.

Adolescent↗
PubMed1999

Modelling the hepatitis C virus epidemic in Australia. Hepatitis C Virus Projections Working Group.

INTRODUCTION: In Australia, to the end of 1997, more than 110,000 people have been diagnosed with hepatitis C virus (HCV) antibodies and reported to State/Territory surveillance systems. The available data indicate that the overwhelming majority (around 80%) of people with HCV antibodies were infected through injecting drug use. METHODS: Models of the HCV epidemic in Australia were developed based on estimates of the pattern of injecting drug use in Australia. Estimates of HCV infections due to injecting drug use thus obtained were then adjusted to allow for HCV infections resulting from other transmission routes. Projections of cirrhosis and hepatocellular carcinoma (HCC) resulting from HCV were obtained by combining modelled HCV incidence with estimates of the progression rates to these outcomes. RESULTS: Based on the models, it was estimated that there were 196,000 (lower and upper limits of 149,000 and 234,000) people in Australia living with HCV antibodies at the end of 1997, with HCV incidence in 1997 estimated to be 11,000 (8500-13,500). It was estimated that 8500 (4000-13,000) people were living with HCV-related cirrhosis in 1997 and that there were 80 (40-125) incident cases of HCV-related HCC. DISCUSSION: Model-based estimates were broadly consistent with other sources of information on the HCV epidemic in Australia. These models suggest that the prevalence of HCV-related cirrhosis and the incidence of HCV-related HCC will more than double in Australia by 2010.

Australia↗
PubMed2003

A golden hamster model for human acute Nipah virus infection.

A predominantly pig-to-human zoonotic infection caused by the novel Nipah virus emerged recently to cause severe morbidity and mortality in both animals and man. Human autopsy studies showed the pathogenesis to be related to systemic vasculitis that led to widespread thrombotic occlusion and microinfarction in most major organs especially in the central nervous system. There was also evidence of extravascular parenchymal infection, particularly near damaged vessels (Wong KT, Shieh WJ, Kumar S, Norain K, Abdullah W, Guarner J, Goldsmith CS, Chua KB, Lam SK, Tan CT, Goh KJ, Chong HT, Jusoh R, Rollin PE, Ksiazek TG, Zaki SR, Nipah Virus Pathology Working Group: Nipah virus infection: Pathology and pathogenesis of an emerging paramyxoviral zoonosis. Am J Pathol 2002, 161:2153-2167). We describe here a golden hamster (Mesocricetus auratus) model that appears to reproduce the pathology and pathogenesis of acute human Nipah infection. Hamsters infected by intranasal or intraperitoneal routes died within 9 to 29 days or 5 to 9 days, respectively. Pathological lesions were most severe and extensive in the hamster brain. Vasculitis, thrombosis, and more rarely, multinucleated endothelial syncytia, were found in blood vessels of multiple organs. Viral antigen and RNA were localized in both vascular and extravascular tissues including neurons, lung, kidney, and spleen, as demonstrated by immunohistochemistry and in situ hybridization, respectively. Paramyxoviral-type nucleocapsids were identified in neurons and in vessel walls. At the terminal stage of infection, virus and/or viral RNA could be recovered from most solid organs and urine, but not from serum. The golden hamster is proposed as a suitable model for further studies including pathogenesis studies, anti-viral drug testing, and vaccine development against acute Nipah infection.

Animals↗
PubMed1978

[Network for the epidemiological survey of the enteroviruses in sewage (author's transl)].

Poliomyelitis still occurs each year in France: 27 cases in 1973, 21 cases in each of 1974 and 1975, 8 cases in 1976. Because of the risk, a survey of the spread of poliovirus in healthy populations and in sewage was organized by the Ministry of Health according to the departmental note DGS/HP/1st/250, 9-2-73. The Laboratoire d'Epidémiologie Virale of the Laboratoire National de la Santé was in charge of the technical aspects of the survey. A preliminary questionnaire was sent to each D.D.A.S.S. (Direction Départementale de l'Action Sanitaire et Sociale) in order to find out the local possibilities for sampling and preliminary treatment of the sewage samples. In 1974, all the samples were sent to the Laboratoire d'Epidémiologie Virale. Since 1975, samples have been sent to a local virology laboratory when available. The sewage samples were concentrated according to SHUVAL's or LUND's methods depending on the local conditions. Both methods tested in our laboratory were found equally efficient. In order to improve their technical laboratory methods, the virologists collaborating in this survey joined together in a working group "Virus et Eaux". For isolating the enteroviruses, we recommend the inoculation of each concentrated sample into primary monkey kidney cells grown in vials; an overlay of agar is added after inoculation. This plaque method allowed us to isolate several strains from one sample. It was possible to demonstrate that polioviruses differing in serotypes and thermosensitivity might be detectable in the same sample. Few of the isolated polioviruses (11/272) showed the same thermoresistance as did the wild strains. Certain enterovirus serotypes are known to be responsible for epidemics of meningitis and neurological disorders. It was of interest to identify non-poliomyelitic enteroviruses isolated from sewage. The study of enterovirus spread in sewage in comparison with that in healthy children is in progress.

Animals↗
PubMed1996

Association of plasma human immunodeficiency virus type 1 RNA level with risk of clinical progression in patients with advanced infection. AIDS Clinical Trials Group (ACTG) 116B/117 Study Team. ACTG Virology Committee Resistance and HIV-1 RNA Working Groups.

Human immunodeficiency virus (HIV)-1 RNA level in plasma was evaluated as a surrogate marker for disease progression in a clinical trial of advanced HIV-1 infection. Baseline HIV-1 RNA level was an independent predictor of disease progression (relative hazard [RH] for each doubling of HIV-1 RNA level, 1.26; 95% confidence interval [CI], 1.03-1.54; P = .02), after adjusting for the week 4 change in HIV-1 RNA level, baseline CD4 cell count, syncytium-inducing phenotype, clinical status at study entry, and therapy randomization. A 50% reduction in HIV-1 RNA level was associated with a 27% decrease in the adjusted risk of disease progression during the study (RH, 0.73; 95% CI, 0.52-1.02; P = .07). The partial validation of HIV-1 RNA as a predictor for clinical end points has implications for the use of HIV-1 RNA in clinical trials and practice.

Acquired Immunodeficiency Syndrome↗
PubMed1994

Specific western blot bands are associated with initial CD4+ lymphocyte counts in human immunodeficiency virus seroconverters. The Navy HIV Working Group.

The Western blot is the most widely used confirmatory test for determining human immunodeficiency virus (HIV) seropositivity. Specific bands in the Western blot indicate antibody responses to various portions of HIV or its precursors, and each is assigned a score from 0 to 3+. While the precise role of humoral antibody responses has not been fully established, specific antibody responses might influence the course of HIV infection. This study investigated the association between antibody reactivity to nine principal Western blot bands and initial CD4+ counts among 877 Navy and Marine Corps personnel during 1988 to 1991. Multiple regression was used to evaluate the strength and significance of the associations and to adjust for age and estimated duration of infection. Strong antibody responses to the p24 core (P < 0.05), p53 reverse transcriptase (P < 0.005), and p55 core precursor (P < 0.0001) antigens were associated with higher initial CD4+ counts, with 33 to 48 additional cells/mm3 associated with each unit increase in the Western blot score, according to a multiple regression analysis which controlled for age and duration of infection (maximum 24 months). By contrast, antibodies to the gp41 transmembrane antigen (P < 0.0001) were associated with lower initial CD4+ counts. Each unit increase in the gp41 band was associated with 76 fewer CD4+ cells/mm3. A negative association was also observed for the gp160 envelope precursor antigen, with each unit increase in reactivity associated with 51 fewer CD4+ cells, although this association was not statistically significant (P = 0.09).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2004

Hepatitis C prevalence--a nationwide serosurvey.

Hepatitis C is the most commonly notified disease in Australia. In 1998 the Hepatitis C Virus Projections Working Group (HCPWG) estimated that there were approximately 210,000 people who had been infected by hepatitis C virus (HCV) in Australia by 2001. Population-based serosurveys are required to validate this estimate. Here we estimate HCV prevalence on the basis of HCV antibody seroprevalence in the Australian national serosurvey. Between 1996 and 1998, 2,800 sera opportunistically collected from pathology laboratories throughout Australia were tested for HCV antibody. National HCV notifications reported from 1991 through 1998 were also assessed. Eighty-one sera were HCV antibody positive, giving an age standardised prevalence of 2.3 per cent (95% CI 1.8%-2.9%). The 20-24 year age group had the highest HCV prevalence, 5.3 per cent (95% CI 3.3%-8.1%) and the male to female ratio was 1.8:1.0. Approximately 111,000 HCV notifications were received from 1991 through 1998. HCV prevalence estimated by the serosurvey is approximately three times higher than cumulative HCV notifications. Age and sex distributions of seroprevalence are broadly consistent with cumulative notification data. These distributions are consistent with the majority of HCV infections in Australia being transmitted by injecting drug use. Very low age specific seroprevalence estimates in the over 50 years age group indicate that there is not a large pool of undiagnosed infection in this age group. The serosurvey provides an estimate of Australian HCV prevalence and baseline data to determine incidence trends, both of which are required for health-care planning.

Adolescent↗
PubMed2004

Monkeypox transmission and pathogenesis in prairie dogs.

During May and June 2003, the first cluster of human monkeypox cases in the United States was reported. Most patients with this febrile vesicular rash illness presumably acquired the infection from prairie dogs. Monkeypox virus was demonstrated by using polymerase chain reaction in two prairie dogs in which pathologic studies showed necrotizing bronchopneumonia, conjunctivitis, and tongue ulceration. Immunohistochemical assays for orthopoxviruses demonstrated abundant viral antigens in surface epithelial cells of lesions in conjunctiva and tongue, with less amounts in adjacent macrophages, fibroblasts, and connective tissues. Viral antigens in the lung were abundant in bronchial epithelial cells, macrophages, and fibroblasts. Virus isolation and electron microscopy demonstrated active viral replication in lungs and tongue. These findings indicate that both respiratory and direct mucocutaneous exposures are potentially important routes of transmission of monkeypox virus between rodents and to humans. Prairie dogs offer insights into transmission, pathogenesis, and new vaccine and treatment trials because they are susceptible to severe monkeypox infection.

Animals↗
PubMed2002

Human surveillance for West Nile virus infection in Ontario in 2000.

BACKGROUND: The first reports of West Nile virus (WNV) infection in the United States in 1999 prompted Ontario to establish a surveillance protocol to monitor for the possible spread of the virus into the province. Surveillance components included evaluation of dead birds, sentinel chickens, mosquito pools and human disease. We report the results of human surveillance in 2000. METHODS: Between July 1 and Oct. 31, 2000, an active surveillance program was undertaken in which designated site coordinators in sentinel hospitals identified patients who met the suspect case definition (fever and fluctuating level of consciousness [encephalopathy], with or without muscle weakness). During the same period, following province-wide distribution of educational material, all other patients tested for WNV antibodies were identified through review of provincial laboratory reports (laboratory-based enhanced passive surveillance). RESULTS: Of the 60 hospitals contacted, 59 agreed to participate in the active surveillance program; 52 provided information on a regular (weekly) basis, and 7 submitted fewer than 8 reports. Thirty-six (61%) of the sentinel sites reported suspect cases. In total, 188 patients were tested (130 identified through active surveillance and 58 through enhanced passive surveillance). Patients identified through active surveillance were more likely than those identified through passive surveillance to meet the suspect case definition (43% [n = 56] v. 7% [n = 4]), to be admitted to hospital (75% [n = 99] v. 16% [n = 9]), to have a longer hospital stay (mean 25 v. 3 days), to have had a second (convalescent) serum sample collected (37% [n = 48] v. 31% [n = 18]), to have had a cerebrospinal fluid (CSF) sample banked (56% [n = 73] v. 14% [n = 8]) and to have had a discharge diagnosis reported (79% [n = 103] v. 28% [n = 16]). Of the 60 patients (32%) who met the suspect case definition, 34 (57% [31 active, 3 passive]) had a discharge diagnosis of encephalitis. Of these, 17 (50% [15 active, 2 passive]) had paired serum samples collected, and 18 (51% [all active]) had a CSF sample banked. The reported causal agents were herpes simplex virus (n = 8), varicelia virus (n = 2), Powassan virus (n = 1), echovirus 30 (n = 1) and group B Streptococcus (n = 1); the cause was unknown in 18 cases. One patient died of encephalitis. The remaining 26 patients who met the suspect case definition were ultimately found to have nonencephalitic infections, vascular events or alcohol- or drug-related illness. The 128 (68%) tested for WNV who did not meet the suspect case definition included 9 patients ultimately discharged with a diagnosis of encephalitis. No cases of WNV infection were identified. INTERPRETATION: Only one-third of the tested patients met the suspect case definition of encephalopathy on admission, and nearly half of them were later found to have another diagnosis; others did not meet the case definition but were later discharged with a diagnosis of encephalitis. This affirms that identification of acute encephalitis on the basis of symptoms at the time of admission is often impossible.

Adult↗
PubMed1989

Final report of the United States Department of Health and Human Services Secretary's Work Group on pediatric human immunodeficiency virus infection and disease: content and implications.

Human immunodeficiency virus (HIV) disease is increasing rapidly in the ranks of the leading causes of death among children. It is already the ninth leading cause of death among children 1 to 4 years of age and the seventh in young people between the ages of 15 and 24 years. If current trends continue, AIDS can be expected to move into the top five leading causes of death in the pediatric and adolescent age group in the next 3 or 4 years. To address this problem and also to provide focus for the US Department of Health and Human Services activities dealing with pediatric AIDS, an intradepartmental work group was established as a central health and human services component. This was done to ensure the best possible use of federal resources on behalf of children and adolescents with AIDS. Its recommendations are the basis of this report.

Acquired Immunodeficiency Syndrome↗
PubMed2001

Guidelines for laboratory test result reporting of human immunodeficiency virus type 1 ribonucleic acid determination. Recommendations from a CDC working group. Centers for Disease Control.

Monitoring human immunodeficiency virus type 1 (HIV-1) ribonucleic acid levels (also known as HIV viral load) has become the standard of care for monitoring response to therapy in HIV-infected patients. In 1999, CDC published updated surveillance case definitions for HIV infection and acquired immunodeficiency syndrome (AIDS) reporting, including positive results of HIV-1 viral detection tests (CDC. Guidelines for national human immunodeficiency virus case surveillance, including monitoring for human immunodeficiency virus infection and acquired immunodeficiency syndrome. MMWR 1999;48[No. RR-131:1-28). Since 1996, an increased number of public and private laboratories have begun performing viral load tests. Results obtained with available test methods are variable, and laboratories present these results in different ways, indicating that guidelines to promote standard practice in reporting of test results are warranted. This report provides guidelines for standardized reporting of viral load test results by licensed laboratories to health-care providers and facilities for public health case reporting of HIV infection and AIDS. Recommended standards were developed through data review, input involving a working group of physicians and laboratorians experienced in viral load testing, and an assessment of laboratory practices. These guidelines were discussed, refined, and endorsed at the annual Human Retrovirus and Hepatitis C Laboratory Testing Conference, held March 6-9, 2000, in Charlotte, North Carolina, with participation of representatives from public health, hospital, independent, and blood-collection-facility laboratories. Adoption of these guidelines by all public and private laboratories that perform HIV viral load testing will improve the quality and usefulness of viral load test results for the physician ordering the test and for reporting to public health departments.

Clinical Laboratory Techniques↗