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At least 883 records · Page 49Linked to original sources
PubMed2005

Exposure to hepatitis C virus induces cellular immune responses without detectable viremia or seroconversion.

Sporadic cases of cell-mediated immunity (CMI) in persons exposed to hepatitis C (HCV) but evidently uninfected have been reported. To further define this, we measured CMI in individuals without evidence of HCV infection, that is, negative for HCV-antibodies (anti-HCV) and RNA, residing in a rural Egyptian community where prevalence of anti-HCV was 24%. Cell-mediated immunity (CMI) measured by interferon-gamma (IFN-gamma) enzyme-linked immunospot (ELISPOT) assay, confirmed by intracellular staining using flow cytometry, against HCV peptides was measured in seronegative individuals with high-risk (HR) and low-risk (LR) exposures to HCV. Thirteen of 71 (18.3%) HR subjects but only 1 of 35 (2.9%) LR subjects had detectable CMI (P = 0.032). These data are compatible with the hypothesis that exposures to HCV may lead to development of HCV-specific CMI without anti-HCV and ongoing viral replication. We speculate induced CMI clears HCV sometimes when anti-HCV is not detectable, and HCV-specific CMI is a useful surrogate marker for exposure to HCV.

Adult↗
PubMed1992

Anti-HIV seroconversion in hemophilia A patient after transfusion of anti-HIV negative blood components.

A Thai male hemophiliac A patient has been anti-HIV seroconverted in the hospital after a 2-year admission for a large infected retroperitoneal hematoma. The source of HIV is thought to be one or more of more than 20,000 units of blood components used during the admission. All were screened as anti-HIV negative. Although he received heat treated factor VIII concentrate before this admission, it was not thought to be the cause. Autologous blood transfusion and HIV antigen screening are suggested as a safer way of blood transfusion.

Adult↗
PubMedDate not supplied

Common clinicopathological features of the patients with chronic hepatitis B virus infection who developed hepatocellular carcinoma after seroconversion to anti-HBs--a consideration of the pathogenesis of HBV-induced hepatocellular carcinoma and a strategy to inhibit it.

BACKGROUND/AIMS: The incidence of hepatocellular carcinoma among patients who have seroconverted to anti-hepatitis B surface antigen (anti-HBs) remains controversial. METHODOLOGY: We report four patients with chronic hepatitis B virus (HBV) infection who had cleared HBsAg and had developed anti-HBs at a later time, but who developed hepatocellular carcinoma (HCC) eventually. RESULTS: The common clinicopathological characteristics of the four patients were: An established diagnosis of precirrhosis or liver cirrhosis more than a decade previously, a long-standing normalization or stabilization at a low level of ALT values due to undetectable HBV DNA by the Amplicore Monitor assay, and a marked reduction of the fibrosis level in the non-tumorous liver obtained at HCC surgery or autopsy compared to the previous histology more than a decade previously. There was no fibrosis in the needle biopsy specimen from one patient. CONCLUSIONS: Our findings suggest that HCC due to HBV can occur in the serologically-cured stage if progression to pre-cirrhosis or cirrhosis already has occurred, where the fibrosis level has improved considerably because of the long-term absence of active HBV viremia and inflammation. Active medical intervention to prevent liver cirrhosis for chronic hepatitis B may have an important role in the inhibition of HCC in patients with chronic hepatitis B.

Adult↗
PubMed2006

Comparison of commercially available and novel West Nile virus immunoassays for detection of seroconversion in pig-tailed macaques (Macaca nemestrina).

We report the assessment and validation of an NS1 epitope-blocking enzyme-linked immunosorbent assay (ELISA) for detection of antibodies to West Nile virus (WNV) in macaques. Sera from naturally infected Macaca nemestrina were tested by ELISA and plaque reduction neutralization test (PRNT). Results were correlated with hemagglutination inhibition (HAI) data. Our results demonstrate that the blocking ELISA rapidly and specifically detects WNV infection in M. nemestrina. In addition, the diagnostic value of 7 commercially available immunoassays (PanBio immunoglobulin [Ig] M ELISA, PanBio IgG ELISA, PanBio immunofluorescence assay (IFA), InBios IgG ELISA, InBios IgM ELISA, Focus Diagnostics IgG ELISA, and Focus Diagnostics IgM ELISA) in M. nemestrina was evaluated and compared with that of the epitope-blocking ELISA. The PanBio IgG ELISA was found to effectively diagnose WNV exposure in M. nemestrina. Further, PanBio IFA slides are fast and reliable screening tools for diagnosing flaviviral exposure in M. nemestrina.

Animals↗
PubMed2006

Detection of Porcine circovirus type 2 viremia and seroconversion in naturally infected pigs in a farrow-to-finish barn.

Porcine serum was assayed by 2 polymerase chain reaction (PCR) protocols (nested PCR [nPCR] and non-nested PCR) and a competitive enzyme-linked immunosorbent assay to determine when Porcine circovirus type 2 (PCV2) viremia and a rise in the serum level of PCV2-specific antibody occurred in pigs raised in a large Canadian farrow-to-finish barn. Eight serial blood samples were collected from each of 40 pigs from 5 to 156 (+/- 1.5) d of age; 6 pigs were removed from the study for various reasons at various times. Viremia was not detected in the samples collected before 72 d of age but was detected in those collected on or after 72 d: of 33 pigs, 7 (21%) had only 1 serum sample positive for PCV2 DNA by nPCR after day 72; 11 (33%) were intermittently positive by nPCR, non-nested PCR, or both between 72 and 156 d; and the remaining 15 (45%) were repeatedly positive (in 2 to 4 samples). The level of serum antibody against PCV2 declined after weaning and increased between 72 and 107 d of age, only after PCV2 was detected in serum. Our results show that PCV2 viremia persists in the presence of elevated levels of PCV2-specific antibody.

Age Factors↗
PubMed1991

[No HCV seroconversion in hemophilia following substitution with virus-inactivated coagulation factor VIII and IX concentrates].

Since 1986 the factor VIII and IX concentrates of the Central Laboratory, Swiss Red Cross Blood Transfusion Service have been virus inactivated with tri-(n-butyl) phosphate and Tween 80. Clinical studies had shown that both preparations were well tolerated and hemostatically effective; no HIV infection was transmitted. However, safety from transmission of non-A/non-B hepatitis could not be shown since the study included no previously untreated patients. In the meantime, a laboratory test has become available which allows retrospective testing for anti-hepatitis C antibodies in frozen sera of the study patients. 5 of the 26 patients, observed during a 2-year follow-up study, had no HCV antibodies before entering the long-term trial. During this trial, each of these 5 patients substituted an average quantity of 40,200 coagulation factor units (7500-69,000) from 45 production lots. None of these 5 patients developed anti-HCV antibodies, nor did any of them show clinical signs of infection with hepatitis. This suggests that virus inactivation using solvent/detergent treatment reduces the risk of transmission of HCV.

Blood Coagulation Disorders↗
PubMedDate not supplied

Absence of HIV-1 and HIV-2 seroconversions in a cohort medical students in a Nigerian medical school.

A cohort of 70, HIV-1 and HIV-2 seronegative medical students were followed up for 30 months, after which 65 were retested for HIV antibody. None of the students was infected by HIV during the period of study. A questionnaire survey carried out showed that all the students had a very good knowledge of HIV, its mode of transmission, control and prevention. Most of the students have never had sex or had a single sex partner and used condoms always or most of the time during sexual intercourse.

Adult↗
PubMed2006

Structured treatment interruptions following immediate initiation of HAART in eight patients with acute HIV-1 seroconversion.

BACKGROUND: The immunological and clinical benefits of structured treatment interruptions (STIs) during primary HIV-1 infection remain largely unclear. PATIENTS AND METHODS: Eight patients identified during primary HIV-1 infection were immediately treated with HAART and underwent subsequent STIs after reaching complete viral suppression of HIV-RNA in peripheral plasma. HAART was re-initiated if either HIV-1 RNA >5000 copies/ml, CD4-cells <200 cells/microl or symptomatic HIV-1 disease was observed. RESULTS: After treatment discontinuation, four of eight patients were able to persistently control HIV-1 viremia below 5000 copies/ml until the last time point of follow-up (median 3 years). CD4-cell counts were within the interquartile range of untreated individuals compared to historical reference data from the MACS cohort. In the remaining study subjects persistent virological control was not reached despite repeated STIs. Moreover, compared to the MACS cohort repetitive virological failures during STIs appeared to induce an accelerated decline of CD4-cells. CONCLUSION: Spontaneous HIV-1 control after treated primary HIV-1 infection was possible in four out of eight individuals, however, if STIs after treated primary infection ameliorate the overall HIV-1 disease progression remains unknown. In the absence of viral control, repetitive viral exposure during STIs might be associated with accelerated decline of CD4-cell counts.

Acute Disease↗