Displaying publications 1 - 20 of 43 in total

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  1. Saeidi A, Ellegård R, Yong YK, Tan HY, Velu V, Ussher JE, et al.
    J. Leukoc. Biol., 2016 Aug;100(2):305-14.
    PMID: 27256572 DOI: 10.1189/jlb.4RU0216-084R
    MAIT cells represent an evolutionarily conserved, MR1-restricted, innate-like cell subset that express high levels of CD161; have a canonical semi-invariant TCR iVα7.2; and may have an important role in mucosal immunity against various bacterial and fungal pathogens. Mature MAIT cells are CD161(hi)PLZF(hi)IL-18Rα(+)iVα7.2(+)γδ-CD3(+)CD8(+) T cells and occur in the peripheral blood, liver, and mucosa of humans. MAIT cells are activated by a metabolic precursor of riboflavin synthesis presented by MR1 and, therefore, respond to many bacteria and some fungi. Despite their broad antibacterial properties, their functional role in persistent viral infections is poorly understood. Although there is an increasing line of evidence portraying the depletion of MAIT cells in HIV disease, the magnitude and the potential mechanisms underlying such depletion remain unclear. Recent studies suggest that MAIT cells are vulnerable to immune exhaustion as a consequence of HIV and hepatitis C virus infections and HIV/tuberculosis coinfections. HIV infection also appears to cause functional depletion of MAIT cells resulting from abnormal expression of T-bet and EOMES, and effective ART is unable to completely salvage functional MAIT cell loss. Depletion and exhaustion of peripheral MAIT cells may affect mucosal immunity and could increase susceptibility to opportunistic infections during HIV infection. Here, we review some of the important mechanisms associated with depletion and functional loss of MAIT cells and also suggest potential immunotherapeutic strategies to restore MAIT cell functions, including the use of IL-7 to restore effector functions in HIV disease.
    Matched MeSH terms: HIV Infections/immunology*
  2. Ng KP, He J, Saw TL, Lyles CM
    Med. J. Malaysia, 2000 Mar;55(1):58-64.
    PMID: 11072492 MyJurnal
    Hepatitis E virus (HEV) is a RNA virus transmitted enterically. A study of anti-HEV antibodies in 145 human immunodeficiency virus type 1 (HIV-1) infected subjects found that 14.4% of them were reactive to anti-HEV antibodies. Anti-HEV IgG and anti-HEV IgM was detected in 10.3% and 4.1% of the subjects respectively. Prevalence of anti-HEV (either IgG or IgM) was similar across all adult ages (p = 0.154), between the three ethnic groups (p = 0.378), and across risk groups (p = 0.120). The results showed that HEV infection in subjects recruited in this study was most likely transmitted via faecal-route.
    Matched MeSH terms: HIV Infections/immunology*
  3. Kosalaraksa P, Boettiger DC, Bunupuradah T, Hansudewechakul R, Saramony S, Do VC, et al.
    J Pediatric Infect Dis Soc, 2017 Jun 01;6(2):173-177.
    PMID: 27295973 DOI: 10.1093/jpids/piw031
    Background.: Regular CD4 count testing is often used to monitor antiretroviral therapy efficacy. However, this practice may be redundant in children with a suppressed human immunodeficiency virus (HIV) viral load.

    Methods: Study end points were as follows: (1) a CD4 count <200 cells/mm3 followed by a CD4 count ≥200 cells/mm3 (transient CD4 <200); (2) CD4 count <200 cells/mm3 confirmed within 6 months (confirmed CD4 <200); and (3) a new or recurrent World Health Organization (WHO) stage 3 or 4 illness (clinical failure). Kaplan-Meier curves and Cox regression were used to evaluate rates and predictors of transient CD4 <200, confirmed CD4 <200, and clinical failure among virally suppressed children aged 5-15 years who were enrolled in the TREAT Asia Pediatric HIV Observational Database.

    Results: Data from 967 children were included in the analysis. At the time of confirmed viral suppression, median age was 10.2 years, 50.4% of children were female, and 95.4% were perinatally infected with HIV. Median CD4 cell count was 837 cells/mm3, and 54.8% of children were classified as having WHO stage 3 or 4 disease. In total, 18 transient CD4 <200 events, 2 confirmed CD4 <200 events, and10 clinical failures occurred at rates of 0.73 (95% confidence interval [95% CI], 0.46-1.16), 0.08 (95% CI, 0.02-0.32), and 0.40 (95% CI, 0.22-0.75) events per 100 patient-years, respectively. CD4 <500 cells/mm3 at the time of viral suppression confirmation was associated with higher rates of both CD4 outcomes.

    Conclusions: Regular CD4 testing may be unnecessary for virally suppressed children aged 5-15 years with CD4 ≥500 cells/mm3.

    Matched MeSH terms: HIV Infections/immunology
  4. Saeidi A, Buggert M, Che KF, Kong YY, Velu V, Larsson M, et al.
    Cell. Immunol., 2015 Nov-Dec;298(1-2):126-33.
    PMID: 26520669 DOI: 10.1016/j.cellimm.2015.10.009
    Understanding the mechanisms involved in cellular immune responses against control of human immunodeficiency virus (HIV) infection is key to development of effective immunotherapeutic strategies against viral proliferation. Clear insights into the regulation of cytotoxic CD8+ T cells is crucial to development of effective immunotherapeutic strategies due to their unique ability to eliminate virus-infected cells during the course of infection. Here, we reviewed the roles of transcription factors, co-inhibitory molecules and regulatory cytokines following HIV infection and their potential significance in regulating the cytotoxic potentials of CD8+ T cells.
    Matched MeSH terms: HIV Infections/immunology*
  5. López M
    AIDS Rev, 2013 Jul-Sep;15(3):190-1.
    PMID: 24002204
    The 7th IAS Conference held in July 2013 in Kuala Lumpur, Malaysia, heard about a number of cases of "functional cure" in people who had started antiretroviral therapy soon after HIV infection, including a German case that can now be added to the "Mississippi baby" report presented at CROI 2012 and 14 individuals of the French VISCONTI cohort. All these persons maintained an undetectable viral load after coming off antiretrovirals.
    Matched MeSH terms: HIV Infections/immunology
  6. Chokephaibulkit K, Kariminia A, Oberdorfer P, Nallusamy R, Bunupuradah T, Hansudewechakul R, et al.
    Pediatr. Infect. Dis. J., 2014 Mar;33(3):291-4.
    PMID: 23942457 DOI: 10.1097/INF.0b013e3182a18223
    More perinatally HIV-infected children in Asia are reaching adolescence.
    Matched MeSH terms: HIV Infections/immunology
  7. Shankar EM, Velu V, Vignesh R, Vijayaraghavalu S, Rukumani DV, Sabet NS
    Microbiol. Immunol., 2012 Aug;56(8):497-505.
    PMID: 22900503 DOI: 10.1111/j.1348-0421.2012.00485.x
    Early defence mechanisms of innate immunity respond rapidly to infection against HIV-1 in the genital mucosa. Additionally, innate immunity optimises effective adaptive immune responses against persistent HIV infection. Recent research has highlighted the intrinsic roles of apolipoprotein B mRNA-editing, enzyme-catalytic, polypeptide-like 3G, tripartite motif-containing protein 5, tetherin, sterile α-motif and histidine/aspartic acid domain-containing protein 1 in restricting HIV-1 replication. Likewise, certain endogenously secreted antimicrobial peptides, namely α/β/θ-defensins, lactoferrins, secretory leukocyte protease inhibitor, trappin-2/elafin and macrophage inflammatory protein-3α are reportedly protective. Whilst certain factors directly inhibit HIV, others can be permissive. Interferon-λ3 exerts an anti-HIV function by activating Janus kinase-signal transducer and activator of transcription-mediated innate responses. Morphine has been found to impair intracellular innate immunity, contributing to HIV establishment in macrophages. Interestingly, protegrin-1 could be used therapeutically to inhibit early HIV-1 establishment. Moreover, chloroquine inhibits plasmacytoid dendritic cell activation and improves effective T-cell responses. This minireview summarizes the recently identified targets for innate immunity-mediated therapies and outlines the challenges that lie ahead in improving treatment of HIV infection.
    Matched MeSH terms: HIV Infections/immunology*
  8. Subha ST, Raman R
    Med. J. Malaysia, 2004 Dec;59(5):688-9.
    PMID: 15889577
    A rare case of Nocardia infection of mastoid is presented in an immunocompromised patient.
    Matched MeSH terms: HIV Infections/immunology*
  9. Ng KP, Saw TL, Baki A, He J, Singh N, Lyles CM
    Int J STD AIDS, 1999 Jun;10(6):401-4.
    PMID: 10414883
    Hema-Strip HIV-1/2 is a one-step rapid test for the detection of anti-HIV-1/2 antibodies in whole blood. The test requires no expensive equipment and the results are available within 10-15 min. Using 72 known HIV-1 positive samples and 780 high-risk prisoners, the sensitivity and specificity of Hema-Strip HIV-1/2 was found to be comparable to microparticle enzyme immunoassay (MEIA). The data also indicated that Hema-Strip HIV-1/2 is an effective alternate testing system to conventional ELISA where the use of ELISA is not suitable and the result of the HIV testing is needed urgently.
    Matched MeSH terms: HIV Infections/immunology*
  10. Yong YK, Shankar EM, Solomon A, Spelman T, Fairley CK, Elliott JH, et al.
    AIDS, 2016 09 10;30(14):2159-68.
    PMID: 27281059 DOI: 10.1097/QAD.0000000000001179
    BACKGROUND: Chronic HIV infection leads to marked depletion of CD4 T cells in the gastrointestinal tract and increased microbial translocation measured by an increase in circulating lipopolysaccharide (LPS) levels. Here, we hypothesized that single-nucleotide polymorphisms (SNPs) in genes encoding the Toll-like receptor 4 (TLR4) and CD14, the principal receptors for LPS, were associated with CD4 T-cell recovery postantiretroviral therapy (ART).

    METHODS: Prospective study of predominantly white HIV-infected participants receiving suppressive ART for at least 12 months. We analysed the CD14 SNPs C-260T and the TLR4 SNPs A+896G, C+1196T. We also determined the levels of LPS and soluble CD14 in plasma samples collected pre-ART and post-ART initiation. CD4 T-cell recovery was assessed by linear mixed models.

    RESULTS: Following ART, individuals with a TT genotype compared with a CT or CC genotype for CD14 C-260T SNP showed higher levels of soluble CD14 (P = 0.008 and 0.003, respectively). The CC genotype for the CD14 C-260T SNP, compared with CT or TT, and the TLR4 SNP (AC/GT), compared with the homozygous genotype (AA/CC), were both independently associated with enhanced long-term CD4 T-cell recovery (>3 months; P HIV-infected individuals post-ART.

    Matched MeSH terms: HIV Infections/immunology*
  11. Ellegård R, Crisci E, Andersson J, Shankar EM, Nyström S, Hinkula J, et al.
    J. Immunol., 2015 Aug 15;195(4):1698-704.
    PMID: 26157174 DOI: 10.4049/jimmunol.1500618
    Mucosa resident dendritic cells (DCs) may represent one of the first immune cells that HIV-1 encounters during sexual transmission. The virions in body fluids can be opsonized with complement factors because of HIV-mediated triggering of the complement cascade, and this appears to influence numerous aspects of the immune defense targeting the virus. One key attribute of host defense is the ability to attract immune cells to the site of infection. In this study, we investigated whether the opsonization of HIV with complement (C-HIV) or a mixture of complement and Abs (CI-HIV) affected the cytokine and chemokine responses generated by DCs, as well as their ability to attract other immune cells. We found that the expression levels of CXCL8, CXCL10, CCL3, and CCL17 were lowered after exposure to either C-HIV or CI-HIV relative to free HIV (F-HIV). DCs exposed to F-HIV induced higher cell migration, consisting mainly of NK cells, compared with opsonized virus, and the chemotaxis of NK cells was dependent on CCL3 and CXCL10. NK cell exposure to supernatants derived from HIV-exposed DCs showed that F-HIV induced phenotypic activation (e.g., increased levels of TIM3, CD69, and CD25) and effector function (e.g., production of IFNγ and killing of target cells) in NK cells, whereas C-HIV and CI-HIV did not. The impairment of NK cell recruitment by DCs exposed to complement-opsonized HIV and the lack of NK activation may contribute to the failure of innate immune responses to control HIV at the site of initial mucosa infection.
    Matched MeSH terms: HIV Infections/immunology*
  12. Ahn JY, Boettiger D, Law M, Kumarasamy N, Yunihastuti E, Chaiwarith R, et al.
    J. Acquir. Immune Defic. Syndr., 2015 Jul 1;69(3):e85-92.
    PMID: 25850606 DOI: 10.1097/QAI.0000000000000634
    Current treatment guidelines for HIV infection recommend routine CD4 lymphocyte (CD4) count monitoring in patients with viral suppression. This may have a limited impact on influencing care as clinically meaningful CD4 decline rarely occurs during viral suppression.
    Matched MeSH terms: HIV Infections/immunology
  13. Ansari AW, Schmidt RE, Shankar EM, Kamarulzaman A
    J Transl Med, 2014;12:341.
    PMID: 25528160 DOI: 10.1186/s12967-014-0341-8
    Even in the era of successful combination antiretroviral therapy (cART), co-infection of Hepatitis C virus (HCV) remains one of the leading causes of non-AIDS-related mortality and morbidity among HIV-positive individuals as a consequence of accelerated liver fibrosis and end-stage liver disease (ESLD). The perturbed liver microenvironment and induction of host pro-inflammatory mediators in response to HIV and HCV infections, play a pivotal role in orchestrating the disease pathogenesis and clinical outcomes. How these viruses communicate each other via chemokine CCL2 and exploit the liver specific cellular environment to exacerbate liver fibrosis in HIV/HCV co-infection setting is a topic of intense discussion. Herein, we provide recent views and insights on potential mechanisms of CCL2 mediated immuno-pathogenesis, and HIV-HCV cross-talk in driving liver inflammation. We believe CCL2 may potentially serve an attractive target of anti-fibrotic intervention against HIV/HCV co-infection associated co-morbidities.
    Matched MeSH terms: HIV Infections/immunology*
  14. Rajasuriar R, Wright E, Lewin SR
    Curr Opin HIV AIDS, 2015 Jan;10(1):35-42.
    PMID: 25415420 DOI: 10.1097/COH.0000000000000118
    The purpose of this review was to summarize recent studies on the effect of early antiretroviral therapy (ART) in HIV-infected patients on markers of immune activation/inflammation, viral persistence and serious non-AIDS events.
    Matched MeSH terms: HIV Infections/immunology*
  15. Kiertiburanakul S, Boettiger D, Lee MP, Omar SF, Tanuma J, Ng OT, et al.
    J Int AIDS Soc, 2014;17:18804.
    PMID: 24598459 DOI: 10.7448/IAS.17.1.18804
    Although antiretroviral therapy (ART) has been rapidly scaled up in Asia, most HIV-positive patients in the region still present with late-stage HIV disease. We aimed to determine trends of pre-ART CD4 levels over time in Asian HIV-positive patients and to determine factors associated with late ART initiation.
    Matched MeSH terms: HIV Infections/immunology
  16. Oyomopito RA, Li PC, Sungkanuparph S, Phanuphak P, Tee KK, Sirisanthana T, et al.
    J. Acquir. Immune Defic. Syndr., 2013 Mar 1;62(3):293-300.
    PMID: 23138836 DOI: 10.1097/QAI.0b013e31827a2e8f
    HIV-1 group M viruses diverge 25%-35% in envelope, important for viral attachment during infection, and 10%-15% in the pol region, under selection pressure from common antiretrovirals. In Asia, subtypes B and CRF01_AE are common genotypes. Our objectives were to determine whether clinical, immunological, or virological treatment responses differed by genotype in treatment-naive patients initiating first-line therapy.
    Matched MeSH terms: HIV Infections/immunology
  17. Chitra P, Bakthavatsalam B, Palvannan T
    Clin. Chim. Acta, 2011 May 12;412(11-12):1151-4.
    PMID: 21300045 DOI: 10.1016/j.cca.2011.01.037
    Acquired immune deficiency syndrome (AIDS) defines the end stage of Human immunodeficiency viral (HIV) infection before the introduction of highly active antiretroviral therapy (HAART). This study was carried out to assess the serum β-2 microglobulin (B2M) as a marker for progression of HIV infected patients undergoing HAART.
    Matched MeSH terms: HIV Infections/immunology*
  18. Zahari MM, Hwan Bae W, Zainal NZ, Habil H, Kamarulzaman A, Altice FL
    Am J Drug Alcohol Abuse, 2010 Jan;36(1):31-8.
    PMID: 20141394 DOI: 10.3109/00952990903544828
    To examine the association between HIV infection and psychiatric disorders among prisoners, where mental illness, substance abuse, and HIV are disproportionately represented.
    Matched MeSH terms: HIV Infections/immunology
  19. Lian YL, Heng BS, Nissapatorn V, Lee C
    Curr. HIV Res., 2007 Sep;5(5):484-9.
    PMID: 17896968
    Attempts to address the significant impact of HAART on medical variables on the Malaysian HIV/AIDS population have yet to be evaluated. This study aims to analyze the proportions of AIDS-defining illnesses (ADIs) before and after HAART. A retrospective study was carried out on 128 new cases of HIV infected patients who first commenced HAART in 2004 at the national HIV reference center. Before commencement of HAART, 76 clinical episodes of ADIs were recorded in 52 patients. Most common being pulmonary Mycobacterium tuberculosis (28.9%), PCP (27.6%) and disseminated and extrapulmonary Mycobacterium tuberculosis (11.8%). During HAART, 8 clinical episodes of ADIs were documented in 7 patients with a median time of onset of 10 weeks after initiation of HAART (range, 4-36 weeks). The median CD4 count at the time of the commencement of HAART for these patients was 11 cells/mm(3). ADIs reported include PCP (2 episodes), disseminated and extrapulmonary Mycobacterium tuberculosis (2 episodes), extrapulmonary cryptococcosis (1 episode), esophageal candidiasis (1 episode), recurrent pneumonia (1 episode) and disseminated or extrapulmonary histoplasmosis (1 episode). Three (37.5%) of these occurred despite a reduction of viral load by at least 2 log(10) and an increased in the CD4 cell count. In conclusion, ADIs can still present after the initiation of successful HAART especially in those with CD4 counts below 100 cells/mm(3). In Malaysia, ADIs are the major causes of HIV/AIDS associated morbidity and mortality, thus increased awareness on the management of these illnesses is warranted especially in the months following HAART.
    Matched MeSH terms: HIV Infections/immunology
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