Showing papers on "Viremia published in 1992"
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TL;DR: Evidence indicates that HCV infection does not elicit protective immunity against reinfection with homologous or heterologous strains, which raises concerns for the development of effective vaccines against HCV.
Abstract: Some individuals infected with hepatitis C virus (HCV) experience multiple episodes of acute hepatitis. It is unclear whether these episodes are due to reinfection with HCV or to reactivation of the original virus infection. Markers of viral replication and host immunity were studied in five chimpanzees sequentially inoculated over a period of 3 years with different HCV strains of proven infectivity. Each rechallenge of a convalescent chimpanzee with the same or a different HCV strain resulted in the reappearance of viremia, which was due to infection with the subsequent challenge virus. The evidence indicates that HCV infection does not elicit protective immunity against reinfection with homologous or heterologous strains, which raises concerns for the development of effective vaccines against HCV.
722 citations
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TL;DR: A competitive polymerase chain reaction (PCR)-based assay for the quantitative detection of human immunodeficiency virus type 1 (HIV-1) viremia was developed and optimized and proved to be useful in the quantitative assay of HIV-1-specific cellular transcripts and proviral DNA sequences from peripheral blood mononuclear cells by using competitor DNA.
Abstract: A competitive polymerase chain reaction (PCR)-based assay for the quantitative detection of human immunodeficiency virus type 1 (HIV-1) viremia was developed and optimized. This method consists of the reverse transcription and subsequent amplification in the same tube of two similar RNA templates, the wild-type template to be quantified and a known amount of the internally deleted synthetic template, both with identical primer recognition sites. The same strategy also proved to be useful in the quantitative assay of HIV-1-specific cellular transcripts and proviral DNA sequences from peripheral blood mononuclear cells by using competitor DNA. The method might be of interest in the study of the precise level of HIV-1 activity during the different clinical phases of the infection and in the simple, fast, and methodologically correct molecular investigation of patients treated with specific antiviral compounds. Images
191 citations
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TL;DR: Pekin ducks, congenitally infected with the duck hepatitis B virus, were used to assess age-dependent variations in viremia, percentage of DHBV-infected hepatocytes, and average levels of DNA replication intermediates in the cytoplasm and of covalently closed circular DNA in the nuclei of infected hepatocytes.
Abstract: A study was carried out to determine some of the factors that might distinguish transient from chronic hepadnavirus infection. First, to better characterize chronic infection, Pekin ducks, congenitally infected with the duck hepatitis B virus (DHBV), were used to assess age-dependent variations in viremia, percentage of DHBV-infected hepatocytes, and average levels of DNA replication intermediates in the cytoplasm and of covalently closed circular DNA in the nuclei of infected hepatocytes. Levels of viremia and viral DNA were found to peak at about the time of hatching but persisted at relatively constant levels in chronically infected birds up to 2 years of age. The percentage of infected hepatocytes was also constant, with DHBV replication in virtually 100% of hepatocytes in all birds. Next, we found that adolescent ducks inoculated intravenously with a large dose of DHBV also developed massive infection of hepatocytes with an early but low-level viremia, followed by rapid development of a neutralizing antibody response. No obvious quantitative or qualitative differences between transiently and chronically infected liver tissue were detected in the intracellular markers of viral replication examined. However, in the adolescent duck experiment, DHBV infection was rapidly cleared from the liver even when up to 80% of hepatocytes were initially infected. In all of these ducks, clearance of infection was accompanied by only a mild hepatitis, with no evidence that massive cell death contributed to the clearance. This finding suggested that mechanisms in addition to immune-mediated destruction of hepatocytes might make major contributions to clearance of infections, including physiological turnover of hepatocytes in the presence of a neutralizing antibody response and/or spontaneous loss of the capacity of hepatocytes to support virus replication.
184 citations
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TL;DR: In vivo reexposure to VZV antigens due to subclinical V zoster viremia or symptomatic VZv reactivation or symptoms of herpes zoster after transplantation may explain the recovery of virus-specific T cell immunity after BMT.
Abstract: Bone marrow transplant (BMT) recipients were evaluated for subclinical varicella-zoster virus (VZV) viremia and symptoms of herpes zoster after transplantation. Viremia was demonstrated by testing peripheral blood mononuclear cells using polymerase chain reaction and was documented in 19% of 37 patients. When reactivation was defined as herpes zoster and/or subclinical VZV viremia, 41% of VZV-seropositive BMT recipients experienced VZV reactivation. None of 12 patients tested before VZV reactivation had T lymphocyte proliferation to VZV antigen (mean stimulation index, 1.0 +/- 0.42 [SD] at less than 100 days; 12.0 +/- 6.03 at greater than 100 days [P = .003]). Among patients tested at greater than 100 days, 5 (63%) of 8 with detectable T cell proliferation had subclinical or clinical VZV reactivation compared with none of 6 who lacked VZV T cell responses. Recovery of VZV-specific cytotoxic T lymphocyte function was observed in 50% of BMT patients, but BMT recipients had significantly fewer circulating cytotoxic T lymphocytes that recognized VZV immediate early protein (P = .03) or glycoprotein I (P = .004) than did healthy VZV immune subjects. In vivo reexposure to VZV antigens due to subclinical VZV viremia or symptomatic VZV reactivation may explain the recovery of virus-specific T cell immunity after BMT.
181 citations
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TL;DR: Transmission of HCV from mother to child by women coinfected with HCV and HIV is demonstrated by women infected with human immunodeficiency virus and the usefulness of PCR for direct and early detection of HC viremia in neonates is indicated.
Abstract: Serum samples from eight pregnant women and their offspring were studied by nested polymerase chain reaction (PCR) for detection of hepatitis C virus (HCV) RNA to evaluate mother-to-child transmission of this virus. The mothers were all infected with human immunodeficiency virus (HIV); none showed symptoms of HCV infection. Anti-HCV antibodies were tested for by recombinant immunoblot assay. HCV viral sequences were found in five of the mothers and four of eight children, three of them at birth. Viremia was persistent in one infant who had chronic transaminase elevation and persistently remained anti-HCV-positive. The other three babies had intermittent viremia; all were asymptomatic and lost anti-HCV antibodies during follow-up. This loss of antibodies was also observed in PCR-negative infants. Thus, these results demonstrate transmission of HCV from mother to child by women coinfected with HCV and HIV. They indicate the usefulness of PCR for direct and early detection of HCV viremia in neonates.
137 citations
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TL;DR: Results suggest that unlike other lentivirus infections in which mature tissue macrophages accumulate cytoplasmic viral RNA to a high level but fail to produce infectious virions, mature tissue Macrophages are the likely primary source of the high titer of viremia present during acute infection with EIAV.
Abstract: In situ hybridization of tissues from two horses infected with the wild-type Wyoming strain of equine infectious anemia virus (EIAV) identified the liver, spleen, lymph nodes, kidney, lung, and adrenal gland as the primary host tissue sites for viral transcription during acute infection. Combined immunohistochemistry, with a monoclonal antibody recognizing a cytoplasmic antigen of equine mononuclear phagocytes, and in situ hybridization for viral RNA identified most infected cells as mature tissue macrophages. In contrast, in situ hybridization of adherent peripheral blood mononuclear cells collected from horses on various days during the first 2 weeks postinfection with the Wyoming strain of EIAV failed to detect any viral RNA in these cells. For the two horses described here, serum reverse transcriptase activity correlated directly with the degree of replication detected in tissue macrophages on the day of sacrifice. These results suggest that unlike other lentivirus infections in which mature tissue macrophages accumulate cytoplasmic viral RNA to a high level but fail to produce infectious virions, mature tissue macrophages are the likely primary source of the high titer of viremia present during acute infection with EIAV. No significant posttranscriptional block of viral replication in tissue macrophages appears to occur with EIAV. Images
119 citations
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TL;DR: The ability of these NYVAC-vectored recombinants to protect pigs from JEV viremia is demonstrated, as well as JEV-neutralizing and hemagglutination-inhibiting antibodies.
113 citations
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TL;DR: Interestingly, despite the increasing viremia level associated with infection progression, the mean transcriptional activity of individual infected cells was found to be only moderately greater in AIDS patients than in asymptomatic infected subjects, and it was noted that quantitation of HIV-1 genomic RNA in plasma samples and quantitation in peripheral blood mononuclear cells appear to be more reliable and sensitive markers of viral activity than quantitative analysis of proviral HIV- 1 sequences in peripheral lymphocytes.
Abstract: Recent molecular evidence indicates that active human immunodeficiency virus type 1 (HIV-1) infection is detectable in both symptomless and symptomatic infected patients. For this main reason, it has been pointed out that precise quantitative analysis of viral activity in vivo is necessary, firstly, for the pathogenetic investigation of the steps relevant to infection progression and, secondly, for better clinical management of HIV-1-infected patients. In this study, the presence of HIV-1 genomic RNA in plasma samples, specific HIV-1 transcripts in peripheral blood mononuclear cells, and proviral DNA sequences were assayed for 33 HIV-1-infected patients (including symptomless and symptomatic subjects) by using a competitive polymerase chain reaction method that allows quantitation of the RNA/DNA target sequences. The quantitative results obtained confirm that transcription of HIV-1 structural genes and complete viral replication occur in all the HIV-1-infected patients independently of the clinical stage. However, although sharp individual differences were detected, a high degree of correlation of the molecular parameters studied with both disease progression and a decrease in the number of CD4+ T lymphocytes was documented. Interestingly, despite the increasing viremia level associated with infection progression, the mean transcriptional activity of individual infected cells was found to be only moderately greater in AIDS patients than in asymptomatic infected subjects. In addition, it was noted that quantitation of HIV-1 genomic RNA in plasma samples and quantitation of specific HIV-1 transcripts in peripheral blood mononuclear cells appear to be more reliable and sensitive markers of viral activity than quantitative analysis of proviral HIV-1 sequences in peripheral lymphocytes.
112 citations
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TL;DR: Data indicate that interferon treatment is frequently associated with the simultaneous fall in titer of viral DNA by several orders of magnitude and the emergence of novel pre-C sequences, some of them preventing HBeAg expression, however, the presumably immune-mediated selection for pre- C mutant viruses and decrease in viremia under interferons treatment appears not to be prognostic for successful or unsuccessful virus elimination.
89 citations
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TL;DR: Second-generation were consistently more sensitive than first-generation assays for the early diagnosis of primary HCV infection, since antibodies remained persistently detectable throughout follow-up regardless of whether viremia was transient or persistent.
Abstract: The sensitivity of first- and second-generation tests for antibody to hepatitis C virus (HCV) and the relationship among the patterns of antibody response and HCV viremia were examined in serial serum samples from 6 chimpanzees experimentally infected with HCV and followed less than or equal to 3 years. HCV infection was transient in 4 chimpanzees and became chronic in 2. All chimpanzees developed antibodies to HCV detectable by second-generation assays, while only 5 of the 6 became positive by first-generation assay. Second-generation were consistently more sensitive than first-generation assays for the early diagnosis of primary HCV infection. The pattern observed with second-generation assays was not influenced by the outcome of HCV infection, since antibodies remained persistently detectable throughout follow-up regardless of whether viremia was transient or persistent. In contrast, the first-generation antibody response was variable: It usually disappeared after loss of viremia, whereas its presence paralleled HCV viremia in chimpanzees with chronic infection.
89 citations
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TL;DR: Results indicate thatHCV replication is maintained in most alcoholics who score positive for anti-HCV Ab in the RIBA2 test, and that HCV viremia can be associated with histological features typical of alcoholic liver disease.
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TL;DR: PCR is a new powerful tool for detection of HCMV infections in blood samples from immunocompromised patients, however, its clinical significance appears to be restricted to the indication of a risk of reactivation of H CMV infection.
Abstract: The presence of human cytomegalovirus (HCMV) DNA in blood was investigated by the polymerase chain reaction (PCR) in 293 blood samples from 86 immunocompromised patients. Of the 86 patients, 23 underwent clinical and virologic follow-up for HCMV infection. In parallel, blood samples were examined for viremia and antigenemia. Concordant results between PCR and assays for viremia and antigenemia were obtained on 124 positive and 110 negative samples, with an overall concordance of 79.8%, while 59 samples (most from patients with HCMV infection) were positive by PCR alone. PCR is a new powerful tool for detection of HCMV infections in blood samples from immunocompromised patients. However, its clinical significance appears to be restricted to the indication of a risk of reactivation of HCMV infection.
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TL;DR: The length of viremia and the proportion of peripheral blood mononuclear cells infected during measles were investigated in 8 adults and virus was identified by syncytia formation and confirmed by immunofluorescent staining.
Abstract: Measles viremia is thought to peak at onset of rash and diminish rapidly over the subsequent 2-3 days. The length of viremia and the proportion of peripheral blood mononuclear cells (PBMC) infected during measles were investigated in 8 adults. Blood was obtained from 7 patients between days 2 and 4 of rash. Five patients had repeat specimens obtained on day 6 or 7, and 1 patient had samples taken on days 6 and 10. Limiting dilutions of PBMC were cultivated with cord blood PBMC and stimulated with phytohemagglutinin. Virus was identified by syncytia formation and confirmed by immunofluorescent staining. Virus was isolated from all 8 patients. Four of 6 patients were still viremic at day 6 or 7 of rash. Titers ranged from 3 to 5623 TCID50/10(5) PBMC. Adults with measles may have prolonged viremia, and a large proportion of PBMC may be infected.
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TL;DR: It is found that the susceptibility of the central nervous system wanes progressively or gradually as a function of the age of the host, this age-dependent resistance being complete by 12 to 14 days of age.
Abstract: A molecular clone of wild mouse ecotropic retrovirus CasBrE (clone 15-1) causes a spongiform neurodegenerative disease with a long incubation period, greater than or equal to 6 months. This virus infects the central nervous system (CNS) at low levels. In contrast, a chimeric virus, FrCasE, containing env and 3' pol sequences of 15-1 in a Friend murine leukemia virus background, infects the CNS at high levels and causes a rapid neurodegenerative disease with an incubation period of only 16 days. With both viruses, the induction of neurologic disease is dependent on inoculation during the perinatal period. Since the length of the incubation period of this disease appears to be a function of the relative level of CNS infection, we have attempted to identify the viral and host factors which determine the relative level of virus infection of the CNS. It was previously shown that the CNS is susceptible to infection only during the perinatal period (M. Czub, S. Czub, F. J. McAtee, and J. L. Portis, J. Virol. 65:2539-2544, 1991). Here we have found that the susceptibility of the CNS wanes progressively or gradually as a function of the age of the host, this age-dependent resistance being complete by 12 to 14 days of age. Utilizing a group of chimeric viruses, we found that the relative level of CNS infection achieved after inoculation of mice at 1 day of age was a function of the kinetics of virus replication and spread in peripheral organs. Viruses which reached peak viremia titers early (5 to 7 days of age) infected the CNS at high levels, and viruses which reached peak titers later infected the CNS at lower levels. Among the group of viruses examined in the current study, the kinetics of peripheral virus replication and spread appeared to be influenced primarily by sequences within the R-U5-5' leader region of the viral genome. These results suggested that the relative level of CNS infection was determined very early in life and appeared to be a function of a dynamic balance between the kinetics of virus replication in the periphery and a progressively developing restriction of virus replication in the CNS.
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TL;DR: The serial divergence of the virus genome in infected individuals, especially in the region encoding the viral envelope protein, may possibly play an important role in developing chronic infection of hepatitis C virus.
Abstract: The influence of viremia on hepatic injury in patients infected with hepatitis C virus was examined by analysis of the relationship between alanine aminotransferase activity and the amount of hepatitis C virus RNA in sequential serum samples from 1 untreated patient with acute hepatitis C and 3 untreated patients with chronic hepatitis C. Semiquantitative analysis by the competitive-reverse-transcription/polymerase-chain-reaction method indicated that the quantity of hepatitis C virus RNA in the serum affected the disease activities of acute and chronic hepatitis C through their natural clinical courses in all these patients. The nucleotide sequence encoding the putative envelope region of the viral genome in the patient with acute hepatitis C was examined. Blood samples taken serially at 2 times of exacerbation of the hepatitis revealed 2 nucleotide mutations, resulting in changes of predicted amino acid residues. This finding suggests that nucleotide mutations in the envelope region of the viral genome may be responsible for the recurrent hepatic injury attributed to recurrence of viremia in patients with hepatitis C. From these aspects, the serial divergence of the virus genome in infected individuals, especially in the region encoding the viral envelope protein, may possibly play an important role in developing chronic infection of hepatitis C virus. © 1992 Wiley-Liss, Inc.
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TL;DR: Quantitative culture of human immunodeficiency virus was performed on 121 plasma samples from 76 HIV-infected individuals to determine the sensitivity of the assay at different stages of disease and to measure the effect of antiviral therapy on plasma viremia.
Abstract: Quantitative culture of human immunodeficiency virus (HIV) was performed on 121 plasma samples from 76 HIV-infected individuals to determine the sensitivity of the assay at different stages of disease and to measure the effect of antiviral therapy on plasma viremia. Plasma virus was detected in 49 of 76 (64%) of patients, primarily those with AIDS and AIDS-related complex (36 of 38) versus asymptomatic subjects (13 of 38) (p less than 0.001, chi 2). Similarly, plasma cultures were more often positive in patients with less than 250 CD4+ T cells per microliter (38 of 40) than in those with greater than 250 CD4+ T cells per microliter (11 of 36) (p less than 0.001, chi 2). Plasma virus cultures were also more likely to be positive in patients with detectable serum p24 antigen (24 of 26) than in those without detectable p24 antigen (25 of 50) (p = 0.0023, chi 2). An effect of zidovudine (ZDV) treatment on plasma viremia was seen in a comparison of treated and untreated patients with less than 250 CD4+ T cells per microliter. Geometric mean titers of plasma viremia from 16 patients treated with ZDV for more than 3 months were significantly lower than titers from 24 untreated patients (10(1.3) versus 10(2.1), p less than 0.05, Student's t test. A comparison of pre- and posttherapy titers in 33 patients receiving antiviral treatment showed that plasma virus was not detectable at either time in 17 patients; there was a fall in plasma virus titer in 12; and titers were unchanged or increased in 4. In patients with advanced disease, plasma viremia is a potential marker of antiviral drug activity.
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TL;DR: A quantitative modification of the shell vial assay was used to investigate cytomegalovirus viremia in solid-organ transplant recipients and it was demonstrated that significant disease sometimes occurred with low-level viresmia.
Abstract: A quantitative modification of the shell vial assay was used to investigate cytomegalovirus viremia in solid-organ transplant recipients. The level of viremia detected in 109 of 407 specimens ranged from 0.02 to 28 infectious foci per 100,000 leukocytes. By using a Poisson model, a technique was developed to determine 95% confidence limits for the measured levels of viremia. These confidence limits were used to determine the level of viremia that could be excluded by culturing a given number of cells. Longitudinal assessment of two transplant recipients revealed different patterns of viremia and demonstrated that significant disease sometimes occurred with low-level viremia. On the basis of the results of the studies, culture of at least 4 x 10(6) leukocytes is recommended for the sensitive detection of cytomegalovirus viremia.
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TL;DR: Perinatal human immunodeficiency virus (HIV) infection is undoubtedly a multifactorial process and the quantity of viremia nor the level of neutralizing antibody in the infected mother is alone predictive of HIV transmission to her offspring.
Abstract: Perinatal human immunodeficiency virus (HIV) infection is undoubtedly a multifactorial process. Neither the quantity of viremia nor the level of neutralizing antibody in the infected mother is alone predictive of HIV transmission to her offspring. Additional cofactors may include the ability of maternal immunity to control the host cell range and rate of viral replication. The placenta probably constitutes an effective barrier to viral transmission unless disrupted by processes such as syphilis. Prevention of such breaks in the trophoblast barrier and efforts to stimulate maternal and newborn HIV-specific immunity may further decrease the perinatal transmission rate.
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TL;DR: Isolation of virus from one foal following intravenous administration of steroids indicates that Ab4p can establish latency and undergo reactivation, and several pathogenic characteristics of Ab4 are retained in the plaque-purified clone, Ab4 p.
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TL;DR: The pattern of mouse hepatitis virus (MHV) JHM dissemination in blood and other tissues was examined during the first 5 days following intranasal inoculation and suggested lymphatic spread of virus to cervical lymph node and mesenteric lymph node as pathways of dissemination in addition to viremia.
Abstract: Using a sensitive infant mouse bioassay to detect infectious virus, the pattern of mouse hepatitis virus (MHV) JHM dissemination in blood and other tissues was examined during the first 5 days following intranasal inoculation. MHV replicated in nasal turbinates of both susceptible BALB and resistant SJL mice from days 1 through 5, but BALB mice had higher titers on days 1 and 2. Viremia was detectable on days 1 through 5 in BALB mice, but only on days 3 and 5 in SJL mice. Transient virus replication occurred in the lungs of both mouse genotypes at 1 and 2 days, then ceased. This correlated with more consistently demonstrable virus in blood collected from the left atrium of the heart, compared to jugular vein, portal vein and right atrial blood. Virus was associated equally with the plasma and cellular fractions of blood on day 3, but was primarily in the buffy coat of the cellular fraction on day 5. Interferon-α/β was detected in serum and spleen, but not liver or brain of BALB mice or in any tissue of SJL mice. BALB serum and spleen interferon was first detected at 36h, peaked between 48 and 72h, and was undetectable by 108h. The distribution of virus in nose, cervical, axillary and mesenteric lymph nodes, spleen, Peyer's patch, thymus, bone marrow and liver was examined at 1, 2, and 3 days. The resulting pattern suggested lymphatic spread of virus to cervical lymph node and mesenteric lymph node as pathways of dissemination in addition to viremia.
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TL;DR: The results imply that the prevalence of HCV viremia may be unexpectedly high among untransfused persons in Thailand, a hypothesis that should be tested in other populations.
Abstract: Aplastic anemia is a rare, life-threatening disease of unknown etiology, with unusually high prevalence in Thailand. It is sometimes associated with non-A, non-B hepatitis (NANBH). The hepatitis C virus (HCV), one of the causes of NANBH, is similar to flaviviridiae, a family of viruses many of whose members cause acute bone marrow suppression. To test the hypothesis that HCV viremia is associated with aplastic anemia among patients in Thailand, we compared 53 untransfused hospitalized aplastic anemia patients and 39 untransfused controls hospitalized for other conditions. We used the polymerase chain reaction to identify HCV viremia in three (5.7%) untransfused patients and two (5.1%) untransfused controls (P = 1.0, by Fisher's two-tailed exact test). Although our data do not exclude the possibility that a small subset of aplastic anemia cases are precipitated by HCV, we conclude that HCV viremia is not generally associated with aplastic anemia in Thailand. Our results also imply that the prevalence of HCV viremia may be unexpectedly high among untransfused persons in Thailand, a hypothesis that should be tested in other populations.
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TL;DR: Simian immunodeficiency virus was used as a model to study the protective efficacy of an immunization regimen currently being evaluated as candidate vaccines against HIV in human subjects, and macaques were shown to be protected from a homologous virus infection.
Abstract: Simian immunodeficiency virus (SIV) was used as a model to study the protective efficacy of an immunization regimen currently being evaluated as candidate vaccines against HIV in human subjects. Four Macaca fascicularis were first immunized with recombinant vaccinia virus expressing the envelope glycoprotein gp160 of SIVmne and then boosted with subunit gp160. Both cell-mediated and humoral immune responses against SIV, including neutralizing antibodies, were elicited. The macaques were shown to be protected from a homologous virus infection as determined by serology, lymphocyte cocultivation, polymerase chain reactions and in vivo transmission analyses. Four unimmunized control animals were readily infected. However, viremia in infected control animals could decrease substantially following the initial phase of infection so that persistent infection might not be readily detectable.
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TL;DR: The observation of viremia in a leukemic child in whom vesicles and hepatitis developed after live varicella vaccination is reported.
Abstract: Live varicella vaccine has been shown to be efficacious for prevention of varicella even in immunocompromised children.1-4 Although the site and extent of viral replication in vaccinated hosts have not been fully defined, vaccinees have developed humoral and cellular immunity.1-5 A viremic phase has been demonstrated in immunocompromised and normal children with natural varicella.6,7 However, a viremic phase has not been reported in vaccinated children. We report our observation of viremia in a leukemic child in whom vesicles and hepatitis developed after live varicella vaccination. MATERIALS AND METHODS Human embryonic lung fibroblasts (HEFs) were used for virus isolation. The cells were grown in 25-cm2 plastic tissue culture flasks containing Eagle9s minimal essential medium with 7.5% fetal bovine serum.
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TL;DR: Murine models with type C murine leukemia viruses have been used to develop major new prophylactic and therapeutic strategies in vaccination, drug therapy of acute virus exposure and chronic viremia, combination therapy, prevention of maternal transmission, and therapy targeted to the central nervous system.
Abstract: Murine models with type C murine leukemia viruses have been used to develop major new prophylactic and therapeutic strategies in vaccination, drug therapy of acute virus exposure and chronic viremia, combination therapy, prevention of maternal transmission, and therapy targeted to the central nervous system. Transgenic mice expressing either the whole human immunodeficiency virus type 1 (HIV-1) provirus or subgenomic sequences allow the in vivo analysis of selected HIV-1 functions. The full replicative cycle of HIV-1 can be studied in human/mouse chimerae which were created by transplanting human hematolymphoid cells into SCID mice. The chimeric SCID mouse models have been used successfully to evaluate anti-HIV-1 drugs. The role of the various murine retrovirus systems in the development of anti-HIV-1 and anti-AIDS therapies is summarized.
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TL;DR: Results demonstrate transmission of HCV from mother to child by women coinfected with HCV and HIV and indicate the usefulness of PCR for direct and early detection ofHCV viremia in neonates.
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TL;DR: HCMV infection diagnosed by the highly sensitive polymerase chain reaction (PCR) technology in blood, urine and skin biopsies of patients after bone marrow transplantation correlated with the reconstitution of peripheral blood lymphocytes and dermal immunohistological alterations to evaluate the interaction of viral infection with the recovery of the immune system.
Abstract: HCMV infection diagnosed by the highly sensitive polymerase chain reaction (PCR) technology in blood, urine and skin biopsies of patients after bone marrow transplantation (BMT) correlated with the reconstitution of peripheral blood lymphocytes and dermal immunohistological alterations to evaluate the interaction of viral infection with the recovery of the immune system, as well as with the induction or aggravation of graftversus-host disease (GVHD). In a prospective study 73% of 63 patients showed viremia at a median time of 25 days after BMT. Only 44% of these cases that also presented with a higher frequency of acute GVHD symptoms developed HCMB disease later on. In the skin, similar immunohistological alternations, as well as frequent primary local HCMV infection before the development of cutaneous signs of GVHD, was found, suggesting the direct involvement of anti-HCMV immune responses in the induction of GVHD-associated organ lesions.
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01 Jan 1992
TL;DR: A variety of immunologic tests currently exists for the detection of viral antibodies and protein antigens, and the presence or absence of viral and nonspecific markers have been used to predict the onset of clinical disease.
Abstract: Persons infected with the human immunodeficiency virus (HIV) have a spectrum of clinical features, ranging from persons who are infected but appear completely healthy to those with rapid disease progression and mortality. All groups, regardless of clinical stage, possess several biologic indicators of viral infection or replication (Figure 5.1). These include viremia, antibodies against viral proteins, circulating viral proteins, and nonspecific markers such as neopterin, beta2-microglobulins, and T4 cell counts. A variety of immunologic tests currently exists for the detection of viral antibodies and protein antigens. These assays have permitted testing programs to protect the blood supply from infected units and to conduct seroprevalence surveys to define the epidemic. More recently, the presence or absence of viral and nonspecific markers have been used to predict the onset of clinical disease.
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01 Jan 1992
TL;DR: Poliomyelitis, an acute disease of the central nervous system (CNS), is caused by poliovirus, a human enterovirus belonging to the Picornaviridae, and is classified into three stable serotypes (types 1, 2, and 3).
Abstract: Poliomyelitis, an acute disease of the central nervous system (CNS), is caused by poliovirus. Poliovirus is a human enterovirus belonging to the Picornaviridae, and is classified into three stable serotypes (types 1, 2, and 3). Poliovirus strains, except for type 2 virulent strains, infect only primates. The poliovirus infection is initiated by ingestion of a virus and its primary multiplication in the alimentary mucosa. The tonsils and Peyer’s patches are invaded early in the course of infection, and extensive viral multiplication occurs in these loci. From these primary sites, the virus moves into deep cervical and mesenteric lymph nodes, and then into the blood. When effective viremia is established, the virus spreads into the CNS, and then paralytic poliomyelitis occurs as a result of destruction of motor neurons in the brain and spinal cord through lytic viral replication.
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TL;DR: The evidence that humoral immune responses in natural HIV-1 infection play a role in clearance of the initial burst of replication as well as in protection against rapid disease progression is summarized.
Abstract: An attempt is made to summarize the evidence that humoral immune responses in natural HIV-1 infection play a role in clearance of the initial burst of replication as well as in protection against rapid disease progression. Therefore, the so-called “asymptomatic carrier state” was defined on the basis of immunological characteristics, such as CD4+ cell number, CD45RA-CD29+ cell number, CD4+ proliferative responses to anti-CD3 mAbs and soluble activation markers, as well as virological characteristics such as the state of the viral genome in the cell, levels of genomic RNA production, antigenemia, viremia and virus phenotype. During natural infection two major classes HIV-1 neutralizing and cell-fusion inhibiting antibodies are elicited. One population directed against mostly continuous epitopes localized in the third variable domain (V3) of the envelope and one against discontinuous epitopes of the envelope. The last population blocks gp120-CD4 attachment, the first does not. The role of each of these popu...