Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.30.2 (endonuclease)
 18,621 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We evaluated the use of the INNO-LIA HIV-1/HIV-2 Ab test (LIA HIV; Innogenetics) for the confirmation of antibodies to human immunodeficiency virus type 1 (HIV-1) and type 2 (HIV-2). The test includes three recombinant HIV-1 proteins: p24 (gag), p17 (gag), and endonuclease (p31; pol), in combination with two synthetic peptides derived from the env gene of HIV-1 and one synthetic peptide selected from the env gene of HIV-2. Analysis of 450 sera from blood donors, 220 sera from patients with non-HIV pathology, and 28 Western blot (WB) p24-only reactive sera revealed no false-positive results, and the rate of indeterminate results was substantially lower than that with WB. Testing of 334 WB-confirmed HIV antibody-positive sera (309 HIV-1; 25 HIV-2) revealed no false-negative results. In two of seven seroconversion panels tested, LIA HIV detected the presence of HIV antibodies before WB did. In the other five panels, LIA HIV and WB confirmed the presence of HIV antibodies in the same sample. The LIA HIV assay therefore appears well suited for routine confirmation of the presence of HIV-1 and HIV-2 antibodies.
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PMID:Confirmation and differentiation of antibodies to human immunodeficiency virus 1 and 2 with a strip-based assay including recombinant antigens and synthetic peptides. 191 62

Sera from the majority of individuals that were positive in an enzyme-linked immunosorbent assay (ELISA) retrovirus (ARV), an isolate of the for antibodies to acquired immune deficiency syndrome (AIDS)-associated retrovirus (ARV), an isolate of the retrovirus identified as the etiologic agent of AIDS, were found to react with a 31,000-dalton protein (p31) in virus Western blot assays. To determine if this 31,000-dalton immunoreactive species originated from the putative endonuclease region of the polymerase (pol) gene of ARV, we cloned this portion of pol into bacterial expression vectors for direct expression and for expression as a fusion protein with human superoxide dismutase. Transformants from both constructions expressed immunoreactive protein detected in immunoblots with an AIDS patient's serum. Extracts from transformants expressing these sequences competed with the binding of antibodies from AIDS patients' sera to the 31,000-dalton protein in virus immunoblots, confirming that viral p31 originated from the endonuclease domain of the ARV polymerase gene. The superoxide dismutase-p31 fusion protein was purified, and an ELISA for detecting antibodies to p31 was developed. The majority (95%) of serum samples obtained from individuals seropositive in the virus ELISA were also positive in the p31 antibody ELISA.
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PMID:Recombinant polypeptide from the endonuclease region of the acquired immune deficiency syndrome retrovirus polymerase (pol) gene detects serum antibodies in most infected individuals. 241 93

Serum samples from 247 patients with positive HIV-1 IgG serology were investigated for specific IgM antibodies. We found that 109 also reacted positively with a least one antigen in an HIV-1 IgM Western Blot and only 31 in an HIV-1 IgM enzyme-linked immunosorbent assay (ELISA). It was shown that in some of the persons, specific IgM antibodies against the gp160/120, p66, p55, gp41, p24, and p17 antigens of the virus are synthesized at some time after infection. IgM antibodies to the endonuclease-related p31 antigen were observed in one serum only. IgM antibodies against the gp160/120, p66, gp41, and p17 antigens seemed to disappear early after infection. Those against the p55 and the p24 antigens were found in 62% and 75% of investigated cases, respectively. A direct correlation between the Western Blot patterns and the IgM ELISA results was not found.
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PMID:Detection of anti-HIV-1 immunoglobulin M antibodies in patients with serologically proved HIV-1 infection. 316 78

Serum samples from 27 patients infected with human T-cell lymphotropic virus type III (14 with acquired immune deficiency syndrome [AIDS] and 13 with AIDS-related complex) were examined for antibodies to viral proteins by the Western blot method and with four different commercial solid-phase enzyme-linked immunosorbent assays (ELISAs). Virus-specific bands on blots at molecular masses of 64, 55, 53, 41, 31, 24, and 17 kilodaltons were observed. Rank correlation matrices were calculated to relate the intensity of viral bands, stage of illness, and ELISA kit optical densities (ODs). Groups of bands tended to covary in intensity: p17, p24, and p55 (gag gene products); p53 and p64 (pol gene products); and p31 (pol/endonuclease gene product) and p41 (env gene product). Blots of sera from AIDS-related complex patients usually showed strong activity against all viral proteins, while those of sera from AIDS patients characteristically showed strong reactivity only at the pol/endonuclease and env bands. For one ELISA kit (Abbott Laboratories, North Chicago, Ill.), ODs correlated well with the env and pol band intensity scores, while ELISA ODs with other kits (from Litton Industries, Sunnyvale, Calif.; Electro-Nucleonics, Inc., Fairfield, N.J.; and E.I. du Pont de Nemours & Co., Inc., Wilmington, Del.) correlated closely with gag band intensity scores. We conclude that human T-cell lymphotropic virus type III Western blot patterns are determined by (i) viral protein processing pathways and (ii) the stage of illness of the patient and may reflect (iii) the ELISA method used for serum screening.
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PMID:Variations in Western blot banding patterns of human T-cell lymphotropic virus type III/lymphadenopathy-associated virus. 354 2

Although human immunodeficiency virus (HIV) infection is progressive, the rate of decline in CD4+ lymphocyte counts varies. The role of immune system components in limiting HIV infection has yet to be defined, but a previous report on the U.S. Navy HIV Seropositive Cohort reported that strong reactivity in the anti-p55 (core precursor), p24 (core) and p53 (reverse transcriptase) Western blot bands was associated with higher CD4+ lymphocyte counts at the first clinical evaluation for HIV. The previous report examined the cross-sectional association between Western blot banding patterns and initial CD4+ lymphocyte counts. This report examines the association between these banding patterns in individuals who progressed rapidly as compared with patterns of patients who did not, based on their trends in repeated CD4+ lymphocyte counts as a marker of progression. Rapid and slower progressors were identified from a cohort of 3414 Navy and Marine Corps personnel who had a first positive HIV Western blot during 1986-1991. For purposes of this study, rapid progressors were defined as individuals whose CD4+ lymphocyte counts declined to < 500 cells/mm3 within 1 year of seroconversion. A total of 325 individuals met these criteria. A comparison group of 63 slower progressors also was identified; this group consisted of those whose CD4+ lymphocyte counts remained at > or = 500 cells/mm3 for a minimum of 5 years of follow-up after their first positive Western blot. Rapid progressors were slightly younger than slower progressors and were more likely to be never married but did not differ significantly from slower progressors in race or sex. Rapid progressors had weaker reactivity in the anti-p55 core precursor (P < 0.0001), p15 core (P < 0.01), gp41 transmembrane (P < 0.01) and p31 endonuclease (P < 0.05) bands on the Western blot. The odds ratio for rapid progressor status associated with weak or absent reactivity was 7.8 in the anti-p55 band and ranged from 2.0 to 3.2 in the anti-p31, p15, and gp41 bands. These associations remained significant after adjustment for age, race, and sex. The p55 association persisted in repeated Western blots during routine clinical evaluation during a period of 5 years after the first positive Western blot. It was concluded that several possible explanations may account for the weaker reactivity of rapid progressors: (i) weak anti-p55 reactivity might have been a marker of early immune system damage; (ii) high concentrations of p55 or related proteins in the serum may have bound the available anti-p55 antibodies in rapid progressors, making them difficult to identify on the Western blot; or (iii) lack of anti-p55, p15, gp41, or p31 reactivity might have allowed more rapid progression.
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PMID:Western blot banding patterns of HIV rapid progressors in the U.S. Navy Seropositive Cohort: implications for vaccine development. Navy Retroviral Working Group. 887 45