Previous studies have identified a central role for HLA-B alleles in influencing control of HIV infection. An alternative possibility is that a small number of HLA-B alleles may have a very strong impact on HIV disease outcome, dominating the contribution of other HLA alleles. Here, we find that even following the exclusion of subjects expressing any of the HLA-B class I alleles (B*57, B*58, and B*18) identified to have the strongest influence on control, the dominant impact of HLA-B alleles on virus set point and absolute CD4 count variation remains significant. However, we also find that the influence of HLA on HIV control in this C-clade-infected cohort from South Africa extends beyond HLA-B as HLA-Cw type remains a significant predictor of virus and CD4 count following exclusion of the strongest HLA-B associations. Furthermore, there is evidence of interdependent protective effects of the HLA-Cw*0401-B*8101, HLA-Cw*1203-B*3910, and HLA-A*7401-B*5703 haplotypes that cannot be explained solely by
Time to Seroconversion in HIV-Exposed Subjects Carrying Protective versus Non Protective KIR3DS1-L1 and HLA-B Genotypes. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
Below is an overview of various Fibromyalgia Treatment options available to the patient. Acupuncture stems from the Chinese philosophy of energy flowing in the meridians that lie below the skin.
UNLABELLED: Human leukocyte antigen B27 (HLA-B27) is associated with protection in human immunodeficiency virus (HIV) and hepatitis C virus (HCV) infection. This protective role is linked to single immunodominant HLA-B27-restricted CD8+ T-cell epitopes in both infections. In order to define the relative contribution of a specific HLA-B27-restricted epitope to the natural course of HCV infection, we compared the biological impact of the highly conserved HCV genotype 1 epitope, for which the protective role has been described, with the corresponding region in genotype 3 that differs in its sequence by three amino acid residues. The genotype 3a peptide was not recognized by CD8+ T cells specific for the genotype 1 peptide. Furthermore, patients with acute or chronic infection with HCV genotype 3a did not mount T-cell responses to this epitope region, and their autologous viral sequences showed no evidence of T-cell pressure. Finally, we found a significantly higher frequency of HLA-B27 positivity in
Human leukocyte antigen class I (HLA I) molecules composed of alpha (heavy) chain, including HLA-A, -B, or -C encoded by HLAgenes, and beta-2-microglobulin (β2M) are membrane proteins on all...
The rapid and extensive spread of the human immunodeficiency virus (HIV) epidemic provides a rare opportunity to witness host-pathogen co-evolution involving humans. A focal point is the interaction between genes encoding human leukocyte antigen (HLA) and those encoding HIV proteins. HLA molecules present fragments (epitopes) of HIV proteins on the surface of infected cells to enable immune recognition and killing by CD8(+) T cells; particular HLA molecules, such as HLA-B*57, HLA-B*27 and HLA-B*51, are more likely to mediate successful control of HIV infection. Mutation within these epitopes can allow viral escape from CD8(+) T-cell recognition. Here we analysed viral sequences and HLA alleles from |2,800 subjects, drawn from 9 distinct study cohorts spanning 5 continents. Initial analysis of the HLA-B*51-restricted epitope, TAFTIPSI (reverse transcriptase residues 128-135), showed a strong correlation between the frequency of the escape mutation I135X and HLA-B*51 prevalence in the 9 study cohorts (P =
Immune control of human immunodeficiency virus type 1 (HIV) infection is typically associated with effective Gag-specific CD8 T-cell responses. We here focus on HLA-B*14, which protects against HIV disease progression, but the immunodominant HLA-B*14-restricted anti-HIV response is Env specific (ERYLKDQQL, HLA-B*14-EL9). A subdominant HLA-B*14-restricted response targets Gag (DRYFKTLRA, HLA-B*14-DA9). Using HLA-B*14/peptide-saporin-conjugated tetramers, we show that HLA-B*14-EL9 is substantially more potent at inhibiting viral replication than HLA-B*14-DA9. HLA-B*14-EL9 also has significantly higher functional avidity ( < 0.0001) and drives stronger selection pressure on the virus than HLA-B*14-DA9. However, these differences were HLA-B*14 subtype specific, applying only to HLA-B*14:02 and not to HLA-B*14:01. Furthermore, the HLA-B*14-associated protection against HIV disease progression is significantly greater for HLA-B*14:02 than for HLA-B*14:01, consistent with the superior antiviral ...
In a study of 114 epidemiologically linked Zambian transmission pairs, we evaluated the impact of human leukocyte antigen class I (HLA-I)-associated amino acid polymorphisms, presumed to reflect cytotoxic T lymphocyte (CTL) escape in Gag and Nef of the virus transmitted from the chronically infected donor, on the plasma viral load (VL) in matched recipients 6 mo after infection. CTL escape mutations in Gag and Nef were seen in the donors, which were subsequently transmitted to recipients, largely unchanged soon after infection. We observed a significant correlation between the number of Gag escape mutations targeted by specific HLA-B allele-restricted CTLs and reduced VLs in the recipients. This negative correlation was most evident in newly infected individuals, whose HLA alleles were unable to effectively target Gag and select for CTL escape mutations in this gene. Nef mutations in the donor had no impact on VL in the recipient. Thus, broad Gag-specific CTL responses capable of driving virus escape in
What is HLA B27 Test : Highlights The human leukocyte antigen B27 blood test is also known as the HLA-B27 test. The HLA-B27 test is used to
Research has shown more than 9 out of 10 people with AS carry a particular gene known as human leukocyte antigen B27 (HLA-B27).. Having this gene doesnt necessarily mean youll develop AS. Its estimated 8 in every 100 people in the general population have the HLA-B27 gene, but most dont have AS.. Its thought having this gene may make you more vulnerable to developing AS. The condition may be triggered by one or more environmental factors, although its not known what these are.. Testing for this gene may be carried out if AS is suspected. However, this test isnt a very reliable method of diagnosing the condition because some people can have the HLA-B27 gene but not have ankylosing spondylitis.. Read about how ankylosing spondylitis is diagnosed.. ...
Research has shown more than 9 out of 10 people with AS carry a particular gene known as human leukocyte antigen B27 (HLA-B27).. Having this gene doesnt necessarily mean youll develop AS. Its estimated 8 in every 100 people in the general population have the HLA-B27 gene, but most dont have AS.. Its thought having this gene may make you more vulnerable to developing AS. The condition may be triggered by one or more environmental factors, although its not known what these are.. Testing for this gene may be carried out if AS is suspected. However, this test isnt a very reliable method of diagnosing the condition because some people can have the HLA-B27 gene but not have ankylosing spondylitis.. Read about how ankylosing spondylitis is diagnosed.. ...
Research has shown more than 9 out of 10 people with AS carry a particular gene known as human leukocyte antigen B27 (HLA-B27).. Having this gene doesnt necessarily mean youll develop AS. Its estimated 8 in every 100 people in the general population have the HLA-B27 gene, but most dont have AS.. Its thought having this gene may make you more vulnerable to developing AS. The condition may be triggered by one or more environmental factors, although its not known what these are.. Testing for this gene may be carried out if AS is suspected. However, this test isnt a very reliable method of diagnosing the condition because some people can have the HLA-B27 gene but not have ankylosing spondylitis.. Read about how ankylosing spondylitis is diagnosed.. ...
Research has shown more than 9 out of 10 people with AS carry a particular gene known as human leukocyte antigen B27 (HLA-B27).. Having this gene doesnt necessarily mean youll develop AS. Its estimated 8 in every 100 people in the general population have the HLA-B27 gene, but most dont have AS.. Its thought having this gene may make you more vulnerable to developing AS. The condition may be triggered by one or more environmental factors, although its not known what these are.. Testing for this gene may be carried out if AS is suspected. However, this test isnt a very reliable method of diagnosing the condition because some people can have the HLA-B27 gene but not have ankylosing spondylitis.. Read about how ankylosing spondylitis is diagnosed.. ...
Polymorphism in the HLA region of a chromosome is the major source of host genetic variability in HIV-1 outcome, but there is limited understanding of the mechanisms underlying the beneficial effect of protective class I alleles such as HLA-B57, -B27, and -B51. Taking advantage of a unique cohort infected with clade B HIV-1 through contaminated blood, in which many variables such as the length of infection, the infecting viral strain, and host genetic background are controlled, we performed a comprehensive study to understand HLA-B51-associated HIV-1 control. We focused on the T cell responses against three dominant HLA-B51-restricted epitopes: Gag327-345(NI9) NANPDCKTI, Pol743-751(LI9) LPPVVAKEI, and Pol283-289(TI8) TAFTIPSI. Mutations in all three dominant epitopes were significantly associated with HLA-B51 in the cohort. A clear hierarchy in selection of epitope mutations was observed through epitope sequencing. L743I in position 1 of epitope LI9 was seen in most B51+ individuals, followed ...
I am running an experiment in which I need to sample all six HLA class I alleles (HLA-A, HLA-B, HLA-C) repeatedly. Is there a dataset online that contains this information? I found this website (http://www.allelefrequencies.net/) but I cannot figure out how to get the data from it in the format that I want. Any help is appreciated. Thank you. EDIT: Sorry, I think the question was a little unclear. What I want to do is have a dataset containing a set of patients, and all 6 of their HLA alleles. Is there such a dataset available somewhere? ...
The high diversity of HLA binding preferences has been driven by the sequence diversity of short segments of relevant pathogenic proteins presented by HLA molecules to the immune system. To identify possible commonalities in HLA binding preferences, we quantify these using a novel measure termed "targeting efficiency," which captures the correlation between HLA-peptide binding affinities and the conservation of the targeted proteomic regions. Analysis of targeting efficiencies for 95 HLA class I alleles over thousands of human proteins and 52 human viruses indicates that HLA molecules preferentially target conserved regions in these proteomes, although the arboviral Flaviviridae are a notable exception where nonconserved regions are preferentially targeted by most alleles. HLA-A alleles and several HLA-B alleles that have maintained close sequence identity with chimpanzee homologues target conserved human proteins and DNA viruses such as Herpesviridae and Adenoviridae most efficiently, while all ...
p>The checksum is a form of redundancy check that is calculated from the sequence. It is useful for tracking sequence updates.,/p> ,p>It should be noted that while, in theory, two different sequences could have the same checksum value, the likelihood that this would happen is extremely low.,/p> ,p>However UniProtKB may contain entries with identical sequences in case of multiple genes (paralogs).,/p> ,p>The checksum is computed as the sequence 64-bit Cyclic Redundancy Check value (CRC64) using the generator polynomial: x,sup>64,/sup> + x,sup>4,/sup> + x,sup>3,/sup> + x + 1. The algorithm is described in the ISO 3309 standard. ,/p> ,p class="publication">Press W.H., Flannery B.P., Teukolsky S.A. and Vetterling W.T.,br /> ,strong>Cyclic redundancy and other checksums,/strong>,br /> ,a href="http://www.nrbook.com/b/bookcpdf.php">Numerical recipes in C 2nd ed., pp896-902, Cambridge University Press (1993),/a>),/p> Checksum:i ...
p>The checksum is a form of redundancy check that is calculated from the sequence. It is useful for tracking sequence updates.,/p> ,p>It should be noted that while, in theory, two different sequences could have the same checksum value, the likelihood that this would happen is extremely low.,/p> ,p>However UniProtKB may contain entries with identical sequences in case of multiple genes (paralogs).,/p> ,p>The checksum is computed as the sequence 64-bit Cyclic Redundancy Check value (CRC64) using the generator polynomial: x,sup>64,/sup> + x,sup>4,/sup> + x,sup>3,/sup> + x + 1. The algorithm is described in the ISO 3309 standard. ,/p> ,p class="publication">Press W.H., Flannery B.P., Teukolsky S.A. and Vetterling W.T.,br /> ,strong>Cyclic redundancy and other checksums,/strong>,br /> ,a href="http://www.nrbook.com/b/bookcpdf.php">Numerical recipes in C 2nd ed., pp896-902, Cambridge University Press (1993),/a>),/p> Checksum:i ...
HLA-B8 molecule functions as a restriction element for M3-W1-B9 CD8+ T cells. (A) T cell recognition of peptide-pulsed HLA-B8-expressing cell lines. (B) Ident
sub type, and it has the same probabilities.. So, even if there is such a big uncertainty in the results, it does give a very crude indication, even for the small reference data set. And, it did match up with the result of the blood test, which was fun, but could just as well have been pure luck.. Bottom line: Its pretty awesome that ordinary people can do stuff like this. I can easily imagine a professional service built around imputation: Patient gets genotyped, its stored on a secure server. The doctor can then, based on a permission scheme, run imputation for things like HLA-B27 as one of many tools when diagnosing. A blood test will always be more accurate than imputation, but is time consuming and costs money. If a doctor could quickly see that the probability of HLA-B27 is low, and depending on the context, it may not be necessary to order a blood test at all.. ...
Specific lysis of HLA-B8-matched EBV-transformed LCLs by M3-W1-B9 CD8+ T cells. (A) Recognition of HLA-B8-matched LCLs by M3-W1-B9 CD8+ T cells. LCLs were c
Protective HLA class I alleles that restrict acute-phase CD8+ T-cell responses are associated with viral escape mutations located in highly conserved regions of human immunodeficiency virus type 1 ...
Supertypes are groups of human leukocyte antigen (HLA) alleles which bind overlapping sets of peptides due to sharing specific residues at the anchor positions-the B and F pockets-of the peptide-bindi
Inically suspected HSR, HLA-B*5701 features a sensitivity of 44 in White and 14 in Black sufferers. ?The specificity in White and Black control subjects was 96
HLA-B27 is a human leukocyte antigen that helps the body differentiate its own cells from foreign substances. A test indicating that HLA-B27 is present means that the patient might have a risk of...
Успешная трансплантация пуповинной крови для лечения анемии Фанкони с использованием преимплантационной генетической диагностики для подбора подходящего по HLA донора
TY - JOUR. T1 - Specific human leukocyte antigen class I and II alleles associated with hepatitis C virus viremia. AU - Kuniholm, Mark H.. AU - Kovacs, Andrea. AU - Gao, Xiaojiang. AU - Xue, Xiaonan. AU - Marti, Darlene. AU - Thio, Chloe L.. AU - Peters, Marion G.. AU - Terrault, Norah A.. AU - Greenblatt, Ruth M.. AU - Goedert, James J.. AU - Cohen, Mardge H.. AU - Minkoff, Howard. AU - Gange, Stephen J.. AU - Anastos, Kathryn. AU - Fazzari, Melissa. AU - Harris, Tiffany G.. AU - Young, Mary A.. AU - Strickler, Howard D.. AU - Carrington, Mary. PY - 2010/5/1. Y1 - 2010/5/1. N2 - Studies of human leukocyte antigen (HLA) alleles and their relation with hepatitis C virus (HCV) viremia have had conflicting results. However, these studies have varied in size and methods, and few large studies assessed HLA class I alleles. Only one study conducted high-resolution class I genotyping. The current investigation therefore involved high-resolution HLA class I and II genotyping of a large multiracial ...
Study to evaluate the utility of prospective HLA-B*5701 screening on the incidence of abacavir hypersensitivity (ABC HSR) in 1800 previously ABC-naive adults with HIV-1 from Europe, Australia and other countries as applicable. The study has two (co-primary) objectives: i) to determine if screening for HLA-B*5701 prior to ABC-containing HAART results in a lower incidence of clinically-suspected HSR versus current standard of care (no genetic screening) and ii) to determine if screening for HLA-B*5701 prior to ABC-containing HAART, results in a significantly lower incidence of immunologically-confirmed HSR versus current standard of care (no genetic screening or patch testing). The study consists of up to a 28-day screening period, a randomised observation period (Day 1 through Week 6) and, for subjects experiencing a suspected ABC HSR and a subset of ABC-tolerant subjects, an epicutaneous patch test (EPT) assessment period. Eligible subjects will be randomised to one of two study arms: a Current ...
Study to evaluate the utility of prospective HLA-B*5701 screening on the incidence of abacavir hypersensitivity (ABC HSR) in 1800 previously ABC-naive adults with HIV-1 from Europe, Australia and other countries as applicable. The study has two (co-primary) objectives: i) to determine if screening for HLA-B*5701 prior to ABC-containing HAART results in a lower incidence of clinically-suspected HSR versus current standard of care (no genetic screening) and ii) to determine if screening for HLA-B*5701 prior to ABC-containing HAART, results in a significantly lower incidence of immunologically-confirmed HSR versus current standard of care (no genetic screening or patch testing). The study consists of up to a 28-day screening period, a randomised observation period (Day 1 through Week 6) and, for subjects experiencing a suspected ABC HSR and a subset of ABC-tolerant subjects, an epicutaneous patch test (EPT) assessment period. Eligible subjects will be randomised to one of two study arms: a Current ...
In this study, we have demonstrated that half of the NK activity of PBL can be inhibited upon HLA-G transfection and that inhibition was mediated, in part at least, by NKAT3. The fetus downregulates classical MHC class I molecules, HLA-A and HLA-B, at the feto-maternal interface ((22)) and, for this reason, the immune system of the mother is not able to attack the placenta by alloreactive T cells. However, the absence of HLA-A and HLA-B molecules potentially renders the fetal cytotrophoblast sensitive for NK recognition and lysis. Moreover, high numbers of CD56+ large granular lymphocytes (LGL) are present in the decidua during early pregnancy; yet, even so, the trophoblast is usually not destroyed. Up to 70% of all decidual lymphocytes show this phenotype ((35)). Based on the two NK receptor theory ((25)), there are two possible explanations for nonrecognition of the fetal cytotrophoblast by maternal NK cells. One is that these cells lack activatory structures for NK cells on their surface ...
IntroductionUnderstanding the mechanisms by which some individuals are able to naturally control HIV-1 infection is an important goal of AIDS research. We here describe the case of an HIV-1+ woman, CASE1, who has spontaneously controlled her viremia for the last 14 of her 20 years of infection.MethodsCASE1 has been clinically monitored since 1993. Detailed immunological, virological and histological analyses were performed on samples obtained between 2009 and 2011.ResultsAs for other Elite Controllers, CASE1 is characterized by low to undetectable levels of plasma HIV-1 RNA, peripheral blood mononuclear cell (PBMC) associated HIV-1 DNA a reduced in vitro susceptibility of target cells to HIV-1 infection. Furthermore, a slow rate of virus evolution was demonstrated in spite the lack of assumption of any antiretroviral agent. CASE1 failed to transmit HIV-1 to either her sexual male partner or to her child born by vaginal delivery. Normal values and ratios of T and B cells were observed, along with ...
HLA-B59 (B59) is an HLA-B serotype. The serotype identifies the more common HLA-B*## gene products. B59 is a hybrid between B*55 and B*51. B59 is more common in Japan, Korea, N. China and Mongolia. (For terminology help see: HLA-serotype tutorial) Marsh SG, Albert ED, Bodmer WF, et al. (2005). "Nomenclature for factors of the HLA system, 2004". Tissue Antigens. 65 (4): 301-69. doi:10.1111/j.1399-0039.2005.00379.x. PMID 15787720. Hildebrand WH, Domena JD, Parham P (1993). "Primary structure shows HLA-B59 to be a hybrid of HLA-B55 and HLA-B51, and not a subtype of HLA-B8". Tissue Antigens. 41 (4): 190-5. doi:10.1111/j.1399-0039.1993.tb02001.x. PMID 8362411. derived from IMGT/HLA Middleton D, Menchaca L, Rood H, Komerofsky R (2003). "New allele frequency database: http://www.allelefrequencies.net". Tissue Antigens. 61 (5): 403-7. doi:10.1034/j.1399-0039.2003.00062.x. PMID 12753660. External link in ,title= (help ...
OBJECTIVE: HLA-B27 is capable of forming in vitro a heavy-chain homodimer structure lacking beta(2)-microglobulin. We undertook this study to ascertain if patients with spondylarthritis express beta(2)-microglobulin-free HLA-B27 heavy chains in the form of homodimers and receptors for HLA-B27 homodimers. METHODS: Expression of HLA-B27 heavy chains by mononuclear cells was analyzed by fluorescence-activated cell sorter staining, Western blotting with the monoclonal antibody HC-10, and 2-dimensional isoelectric focusing. Fluorescence-labeled tetrameric complexes of HLA-B27 heavy-chain homodimers were constructed in which each dimer comprised one His-tagged heavy chain and one biotinylated heavy chain, and were used to stain patient and control mononuclear cells and transfected cell lines. RESULTS: Patients with spondylarthritis expressed cell-surface HLA-B27 homodimers. Populations of synovial and peripheral blood monocytes, and B and T lymphocytes from patients with spondylarthritis, and controls carried
Kawashima Y., Pfafferott K., Frater J., Matthews P., Payne R., Addo M., Gatanaga H., Fujiwara M., Hachiya A., Koizumi H., Kuse N., Oka S., Duda A., Prendergast A., Crawford H., Leslie A., Brumme Z., Brumme C., Allen T., Brander C., Kaslow R., Tang J., Hunter E., Allen S., Mulenga J., Branch S., Roach T., John M., Mallal S., Ogwu A., Shapiro R., Prado J.G., Fidler S., Weber J., Pybus O.G., Klenerman P., Ndungu T., Phillips R., Heckerman D., Harrigan P.R., Walker B.D., Takiguchi M., Goulder P. (2009) Adaptation of HIV-1 to human leukocyte antigen class I. Nature ...
HLA-B57 (B57) is an HLA-B serotype. B57 is a split antigen from the B17 broad antigen, the sister serotype B58. The serotype identifies the more common HLA-B*58 gene products. (For terminology help see: HLA-serotype tutorial) Like B58, B57 is involved in drug-induced inflammatory skin disorders. HLA-B*5701 is associated with drug-induced inflammatory disease of the skin. Individuals with B57 are more sensitive to the drug abacavir. Abacavir is an antiretroviral drug used in treatment of HIV, however in sensitive individuals fever, skin rash, fatigue, gastrointestinal symptoms such as nausea, vomiting, diarrhea or abdominal pain and respiratory symptoms such as pharyngitis, dyspnea, or cough can develop. FDA has advised that people from at-risk ethnic groups, (see table on the left) be screened prior to drug-therapy. [Note: phenotype frequencies are roughly double allele frequencies -tabled values- when allele frequency is less than 30%] Ways JP, Coppin HL, Parham P (1985). "The complete primary ...
Thus, one possible explanation for the observed HLA associations with HIV disease outcome could be that the specific HIV epitopes presented by different HLA-B molecules have an important bearing on the effectiveness of the CD8+ T-cell response. A common feature of the immunodominant epitopes presented by HLA alleles that are associated with slow HIV disease progression, HLA-B*27/*57/*5801/*8101, is that these are all within the highly abundant and conserved Gag capsid (p24) protein [45, 57-61]. Group B streptococcal disease in infants: a case control study. Archives of Disease in Childhood. 2009;94:674-80. 26. Merenstein GB. Neonatal sepsis. Current Opinion in Infectious Diseases. 1992;5:553-7. 27. Johnson CE, Whitwell JK, Pethe K, Saxena K, Super DM. Term newborns who are at risk for sepsis: are lumbar punctures necessary? Pediatrics. 1997;99:E10. 28. Fielkow S, Reuter S, Gotoff SP. Cerebrospinal fluid examination in symptom-free infants with risk factors for infection. J Pediatr. ...
Abacavir is a nucleoside reverse transcriptase inhibitor used for combination antiretroviral therapy for treating human immunodeficiency virus (HIV) infection. An adverse effect from abacavir is a treatment-limiting hypersensitivity reaction, which can be severe and potentially life-threatening. Abacavir-induced hypersensitivity reaction has been associated with the presence of the major histocompatibility complex class I allele HLA-B*5701. A screening test for the HLA-B*5701 allele can assist clinicians to identify patients who are at risk of developing a hypersensitivity reaction to abacavir.. ...
In studies of antigenic peptide presentation, we have found a healthy volunteer whose lymphoblastoid cells were unable to present three different virus-derived epitopes to cytotoxic T lymphocytes (CTL) despite expressing the correct restricting HLA-B27 molecules on the cell surface. B cell lines were established from other members of the donors family, including individuals suffering from ankylosing spondylitis and related diseases, and were tested for their ability to function as target cells in the same assay. None of the eight B cell lines that expressed HLA-B27 presented a known peptide epitope to CTL. However, cells from a family member that expressed HLA-B8 could present an epitope peptide restricted by that molecule. The B27 molecule in this family proved to be the B2702 subtype on isoelectric focusing gels, appearing in exactly the same position as B2702 from other cell lines that did present the peptide. To exclude mutations resulting in noncharged amino acid substitutions, cDNA coding ...
In ecology, disease tolerance is defined as an evolutionary strategy of hosts against pathogens, characterized by reduced or absent pathogenesis despite high pathogen load. To our knowledge, tolerance has to date not been quantified and disentangled from host resistance to disease in any clinically relevant human infection. Using data from the Swiss HIV Cohort Study, we investigated if there is variation in tolerance to HIV in humans and if this variation is associated with polymorphisms in the human genome. In particular, we tested for associations between tolerance and alleles of the Human Leukocyte Antigen (HLA) genes, the CC chemokine receptor 5 (CCR5), the age at which individuals were infected, and their sex. We found that HLA-B alleles associated with better HIV control do not confer tolerance. The slower disease progression associated with these alleles can be fully attributed to the extent of viral load reduction in carriers. However, we observed that tolerance significantly varies across HLA
The human leukocyte antigen (HLA) is a gene complex encoding the major histocompatibility complex (MHC) proteins in humans. The complex is located within the 6p21.3 region on the short arm of human chromosome 6. These genes are highly polymorphic, which means there are many different HLA alleles. More information of HLA and HLA alleles can be found on hla.alleles.org and The IMGT/HLA Database. This is an attempt to plot the rapidly increasing number of HLA alleles over time, with data directly parsed from the IMGT/HLA Statistics page. This notebook file, described below, can be downloaded here.. ...
Results. We found 10.1% of UA (38/375) versus 7.2% (403/5584) of controls were HLA-B27-positive (OR 1.5, 95% CI 1.0-2.1; p = 0.037). HLA-B27-positive patients with UA had more SpA features than HLA-B27-negative patients (mean 1.6, SD 1.0, and 0.9 SD 0.6; p , 0.001), but patients with SpA had significantly more SpA features (mean 4.5, SD 1.5; p , 0.001). Family history and preceding infection were features more common in HLA-B27-positive than in HLA-B27-negative UA (15.8% vs 1.3%, p = 0.04 and 15.8% vs 2.6%, p = 0.04). After HLA-B27 testing, 21 additional patients (5.6%) with UA could potentially have been classified with pSpA according to the ASAS criteria. ...
TY - JOUR. T1 - The occurrence of HLA‐B46 in two Caucasoid families. AU - Hart, J. M.. AU - Zemmour, J.. AU - Schmeckpeper, B. J.. AU - Parham, P.. AU - Wood, W. W.. AU - Hopkins, K. A.. AU - Leffell, M. S.. AU - Bias, W. B.. PY - 1993/1. Y1 - 1993/1. KW - DNA sequence of Caucasoid HLA‐B46. KW - HLA distribution in populations. KW - HLA‐B46 in non‐orientals. KW - gene flow of HLA antigens. UR - http://www.scopus.com/inward/record.url?scp=0027447465&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=0027447465&partnerID=8YFLogxK. U2 - 10.1111/j.1399-0039.1993.tb01977.x. DO - 10.1111/j.1399-0039.1993.tb01977.x. M3 - Article. C2 - 8456442. AN - SCOPUS:0027447465. VL - 41. SP - 47. EP - 50. JO - HLA. JF - HLA. SN - 2059-2302. IS - 1. ER - ...
In a population of jaguars, a gene with two alleles encodes the fur color. Allele B causes melanism (dark fur) and is dominant over allele b, which results in light colored fur. Suppose that there is a migration event, producing a ...
The HLA-B*52:01 and -C*12:02-restricted CTLs strongly suppress HIV-1 replication resulting in slower disease progression. In contrast, the HLA-B*52:01-C*12:02 haplotypes are suscep ...
May 2, 2017 ... Sabrina Gmuca, Rui Xiao, [. ... HLA-B27 positivity in this group of children also seems to vary by geographic location. Cohorts from India and ... ...
SCOPe: Structural Classification of Proteins - extended database, and ASTRAL compendium for protein structure and sequence analysis
Several genetic changes have been found to increase the risk of SJS/TEN in response to triggering factors such as medications. Most of these changes occur in genes that are involved in the normal function of the immune system.. The genetic variations most strongly associated with SJS/TEN occur in the HLA-B gene. This gene is part of a family of genes called the human leukocyte antigen (HLA) complex. The HLA complex helps the immune system distinguish the bodys own proteins from proteins made by foreign invaders (such as viruses and bacteria). The HLA-B gene has many different normal variations, allowing each persons immune system to react to a wide range of foreign proteins. Certain variations in this gene occur much more often in people with SJS/TEN than in people without the condition.. Studies suggest that the HLA-B gene variations associated with SJS/TEN cause the immune system to react abnormally to certain medications. In a process that is not well understood, the drug causes immune ...
In this review we detected 16 alleles groups significantly associated with risk of HIV MTCT and/or with progression of disease in HIV-infected children (Table 1). HLA-B homozygosis was assumed as one allele group, HLA-B*57 allele was the most frequent allele showing a protective effect against the risk for HIV infection in children. This protective effect was detected in four different studies.10,11,21,22 Four alleles groups (HLA-B*27, B*57, B*58, B*81) were significantly associated with slower progression of HIV infection in children while six alleles groups (HLA-B*8, B*18, B*42, B*44, B*49, B*53) were associated with reduced risk of HIV-1 MTCT (Table 1). HLA-B*53:01 allele was associated with reduced risk of HIV-1 MTCT in the study by Winchester et al., but was also associated to rapid disease progression in the study by Gao et al.12,23. On the other hand, five alleles groups (HLA-B*18, B*35, B*45, B*58, B*homozygosis) were related to rapid HIV progression in children, and six alleles groups ...
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Temporal effect of HLA-B*57 on viral control during primary HIV-1 infection. A recent study by Vaidya et al. examined the role of HLA-B alleles in viral control during the acute phase of HIV-1 infection and establishment of the early viral load set point (VLSP). The research concluded that the effect of HLA-B*57 on viral control is more evident during later stage of primary HIV-1 infection. The finding suggest that the mechanism of HLA-B*57 effect on viral control manifests during first several months after HIV-1 infection, which is a critical period in pathogenesis. Polymorphisms at position 97 of HLA-B is found to be the key factor. Source: Vaidya SA, Streeck H, Beckwith N, et al. Retrovirology. 2013;10:139. doi: 10.1186/1742-4690-10-139.. Advanced HIV Disease at Entry into HIV Care and Initiation of Antiretroviral Therapy during 2006-2011: Findings from Four Sub-Saharan African Countries. Early diagnosis, prompt enrollment and engagement in HIV care are the key to timely antiretroviral ...