Displaying publications 21 - 40 of 55 in total

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  1. 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*
  2. 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*
  3. Chow WZ, Lim SH, Ong LY, Yong YK, Takebe Y, Kamarulzaman A, et al.
    PLoS One, 2015;10(9):e0137281.
    PMID: 26335136 DOI: 10.1371/journal.pone.0137281
    Human immunodeficiency virus type 1 (HIV-1) subtypes have been shown to differ in the rate of clinical progression. We studied the association between HIV-1 subtypes and the rate of CD4+ T-cell recovery in a longitudinal cohort of patients on combination antiretroviral therapy (cART). We studied 103 patients infected with CRF01_AE (69%) and subtype B (31%) who initiated cART between 2006 and 2013. Demographic data, CD4+ T-cell counts and HIV-1 viral load were abstracted from patient medical charts. Kaplan-Meier was used to estimate the time to CD4+ T-cell count increase to ≥350 between subtypes and effects of covariates were analysed using Cox proportional hazards. An 87% of the study population were male adults (mean age of 38.7 years old). Baseline CD4+ T-cell counts and viral loads, age at cART initiation, sex, ethnicity and co-infection did not differ significantly between subtypes. A shorter median time for CD4+ T-cell count increase to ≥350 cells/μL was observed for CRF01_AE (546 days; 95% confidence interval [CI], 186-906 days; P = .502) compared to subtype B (987 days; 95% CI, 894-1079 days). In multivariate analysis, female sex was significantly associated with a 2.7 times higher chance of achieving CD4+ T-cell recovery (adjusted hazard ratio [HR], 2.75; 95% CI, 1.21-6.22; P = .025) and both baseline CD4+ T-cell count (P = .001) and viral load (P = .001) were important predictors for CD4+ T-cell recovery. Immunological recovery correlated significantly with female sex, baseline CD4+ T-cell counts and viral load but not subtype.
    Matched MeSH terms: HIV Infections/immunology
  4. Tan DB, Yong YK, Tan HY, Kamarulzaman A, Tan LH, Lim A, et al.
    HIV Med, 2008 May;9(5):307-16.
    PMID: 18400078 DOI: 10.1111/j.1468-1293.2008.00565.x
    A proportion of HIV patients beginning antiretroviral therapy (ART) develop immune restoration disease (IRD). Immunological characteristics of IRD were investigated in a cohort of HIV patients beginning therapy in Kuala Lumpur, Malaysia.
    Matched MeSH terms: HIV Infections/immunology*
  5. Kared H, Tan SW, Lau MC, Chevrier M, Tan C, How W, et al.
    Nat Commun, 2020 02 10;11(1):821.
    PMID: 32041953 DOI: 10.1038/s41467-020-14442-6
    The diversity of the naïve T cell repertoire drives the replenishment potential and capacity of memory T cells to respond to immune challenges. Attrition of the immune system is associated with an increased prevalence of pathologies in aged individuals, but whether stem cell memory T lymphocytes (TSCM) contribute to such attrition is still unclear. Using single cells RNA sequencing and high-dimensional flow cytometry, we demonstrate that TSCM heterogeneity results from differential engagement of Wnt signaling. In humans, aging is associated with the coupled loss of Wnt/β-catenin signature in CD4 TSCM and systemic increase in the levels of Dickkopf-related protein 1, a natural inhibitor of the Wnt/β-catenin pathway. Functional assays support recent thymic emigrants as the precursors of CD4 TSCM. Our data thus hint that reversing TSCM defects by metabolic targeting of the Wnt/β-catenin pathway may be a viable approach to restore and preserve immune homeostasis in the context of immunological history.
    Matched MeSH terms: HIV Infections/immunology
  6. 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*
  7. Pakianathan MR, Kamarulzaman A, Ismail R, McMillan A, Scott GR
    AIDS, 1999 Sep 10;13(13):1787-8.
    PMID: 10509585
    Matched MeSH terms: HIV Infections/immunology*
  8. Amar HS, Ho JJ, Mohan AJ
    J Paediatr Child Health, 1999 Feb;35(1):63-6.
    PMID: 10234638
    OBJECTIVE: To determine the community prevalence of human immunodeficiency virus (HIV) in women at the time of delivery in a Malaysian setting.

    METHODOLOGY: Cord blood samples from a pilot screening programme for congenital hypothyroidism in 1995 at Ipoh city and surrounding district hospitals were screened anonymously for HIV 1 and 2. HIV status was determined using chemiluminescent technology. Positive samples were retested using the Genelavia Mixt assay.

    RESULTS: A total of 4927 samples were tested. The ethnic breakdown included 51.7% Malays, 18.9% Chinese, 14.3% Indian, 2.3% Others and 12.9% unknown. The geographical distribution of samples was 73.9% urban, 24.2% rural and 1.9% unknown. The seroprevalence of HIV positivity was 3.25 per 1000 deliveries (95% CI: 1.92-5.16). Seroprevalence was higher for samples from rural and Malay mothers.

    CONCLUSION: The high seroprevalence in this study suggests that the spread of HIV is far wider than that anticipated by mandatory national reporting. It also supports antenatal screening and the use of antiretroviral therapy as an important strategy to reduce perinatal transmission.

    Matched MeSH terms: HIV Infections/immunology
  9. Yap SH, Abdullah NK, McStea M, Takayama K, Chong ML, Crisci E, et al.
    PLoS One, 2017;12(10):e0186000.
    PMID: 29016635 DOI: 10.1371/journal.pone.0186000
    BACKGROUND: Co-infections with human herpesvirus (HHV) have been associated with residual chronic inflammation in antiretroviral (ART)-treated human immunodeficiency virus (HIV)-infected individuals. However, the role of HHV in modulating the tryptophan-kynurenine pathway and clinical outcomes in HIV-infected individuals is poorly understood. Thus, we investigated the seroprevalence of four common HHVs among treated HIV-infected participants and their impact on kynurenine/tryptophan (K/T) ratio and long-term CD4 T-cell recovery in HIV/HHV co-infected participants.

    METHOD: In this cross-sectional study, HIV-infected participants receiving suppressive ART for a minimum of 12 months were recruited from the University Malaya Medical Centre (UMMC), Malaysia. Stored plasma was analyzed for CMV, VZV, HSV-1 and HSV-2 IgG antibody levels, immune activation markers (interleukin-6, interferon-γ, neopterin and sCD14), kynurenine and tryptophan concentrations. The influence of the number of HHV co-infection and K/T ratio on CD4 T-cell recovery was assessed using multivariate Poisson regression.

    RESULTS: A total of 232 HIV-infected participants were recruited and all participants were seropositive for at least one HHV; 96.1% with CMV, 86.6% with VZV, 70.7% with HSV-1 and 53.9% with HSV-2. K/T ratio had a significant positive correlation with CMV (rho = 0.205, p = 0.002), VZV (rho = 0.173, p = 0.009) and a tendency with HSV-2 (rho = 0.120, p = 0.070), with CMV antibody titer demonstrating the strongest modulating effect on K/T ratio among the four HHVs assessed in SOM analysis. In multivariate analysis, higher K/T ratio (p = 0.03) and increasing number of HHV co-infections (p<0.001) were independently associated with poorer CD4 T-cell recovery following 12 months of ART initiation.

    CONCLUSION: Multiple HHV co-infections are common among ART-treated HIV-infected participants in the developing country setting and associated with persistent immune activation and poorer CD4 T-cell recovery.

    Matched MeSH terms: HIV Infections/immunology
  10. Jiamsakul A, Sungkanuparph S, Law M, Kantor R, Praparattanapan J, Li PC, et al.
    J Int AIDS Soc, 2014;17:19053.
    PMID: 25141905 DOI: 10.7448/IAS.17.1.19053
    First-line antiretroviral therapy (ART) failure often results from the development of resistance-associated mutations (RAMs). Three patterns, including thymidine analogue mutations (TAMs), 69 Insertion (69Ins) and the Q151M complex, are associated with resistance to multiple-nucleoside reverse transcriptase inhibitors (NRTIs) and may compromise treatment options for second-line ART.
    Matched MeSH terms: HIV Infections/immunology
  11. Saeidi A, Ellegård R, Yong YK, Tan HY, Velu V, Ussher JE, et al.
    J Leukoc Biol, 2016 08;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*
  12. 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*
  13. Oyomopito RA, Li PC, Sungkanuparph S, Phanuphak P, Tee KK, Sirisanthana T, et al.
    J Acquir Immune Defic Syndr, 2013 Mar 01;62(3):293-300.
    PMID: 23138836 DOI: 10.1097/QAI.0b013e31827a2e8f
    BACKGROUND: 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.

    METHODS: Prospectively collected longitudinal data from patients in Thailand, Hong Kong, Malaysia, Japan, Taiwan, and South Korea were provided for analysis. Covariates included demographics, hepatitis B and C coinfections, baseline CD4 T lymphocyte count, and plasma HIV-1 RNA levels. Clinical deterioration (a new diagnosis of Centers for Disease Control and Prevention category B/AIDS-defining illness or death) was assessed by proportional hazards models. Surrogate endpoints were 12-month change in CD4 cell count and virologic suppression post therapy, evaluated by linear and logistic regression, respectively.

    RESULTS: Of 1105 patients, 1036 (93.8%) infected with CRF01_AE or subtype B were eligible for inclusion in clinical deterioration analyses and contributed 1546.7 person-years of follow-up (median: 413 days, interquartile range: 169-672 days). Patients >40 years demonstrated smaller immunological increases (P = 0.002) and higher risk of clinical deterioration (hazard ratio = 2.17; P = 0.008). Patients with baseline CD4 cell counts >200 cells per microliter had lower risk of clinical deterioration (hazard ratio = 0.373; P = 0.003). A total of 532 patients (48.1% of eligible) had CD4 counts available at baseline and 12 months post therapy for inclusion in immunolgic analyses. Patients infected with subtype B had larger increases in CD4 counts at 12 months (P = 0.024). A total of 530 patients (48.0% of eligible) were included in virological analyses with no differences in response found between genotypes.

    CONCLUSIONS: Results suggest that patients infected with CRF01_AE have reduced immunologic response to therapy at 12 months, compared with subtype B-infected counterparts. Clinical deterioration was associated with low baseline CD4 counts and older age. The lack of differences in virologic outcomes suggests that all patients have opportunities for virological suppression.

    Matched MeSH terms: HIV Infections/immunology
  14. Mohamad Isa II, Abu Bakar S, Ab Rahman AK
    J Med Virol, 2020 08;92(8):1173-1181.
    PMID: 31957025 DOI: 10.1002/jmv.25680
    The impact of sociodemographic and clinical factors on immune recovery and viral load suppression among HIV-1 positive patients treated with HAART particularly in Malaysia is largely unknown. This cross-sectional study enrolled 170 HIV-1-infected individuals of three major ethnicities who attended three HIV outpatient clinics in Malaysia. Questionnaire was used to obtain sociodemographic data while CD4 count and viral load data were gathered from hospital's record. Multiple factors were assessed for their predictive effects on CD4 count recovery (≥500 cells/mm3 ) and viral load suppression (≤50 copies/mL) using binary logistic regression. Most of the subjects were male (149/87.6%), in the age group 30 to 39 years old (78/45.9%) and got infected via homosexual contact (82/48.2%). Indians were associated with 11 times higher chance for CD4 recovery as compared to Malays at 8 to 12 months of HAART (adjusted OR: 10.948, 95% CI: 1.873, 64.001, P = .008). Viral load suppression was positively influenced by intravenous drug use (IVDU) status (adjusted OR: 35.224, 95% CI: 1.234, 1000.489, P = .037) at 4 to 6 months of HAART. Higher pretreatment CD4 count was a positive predictor for both initial immunological and virological responses while higher pretreatment viral load was a negative predictor for virological suppression only. In conclusion, ethnicity plays a significant role in determining early immune reconstitution in Malaysia, besides pretreatment CD4 count. Further studies are needed to identify possible biological factors underlying this association.
    Matched MeSH terms: HIV Infections/immunology*
  15. Lee SC, Chua LL, Yap SH, Khang TF, Leng CY, Raja Azwa RI, et al.
    Sci Rep, 2018 09 24;8(1):14277.
    PMID: 30250162 DOI: 10.1038/s41598-018-32585-x
    We explored the gut microbiota profile among HIV-infected individuals with diverse immune recovery profiles following long-term suppressive ART and investigated the relationship between the altered bacteria with markers of immune dysfunction. The microbiota profile of rectal swabs from 26 HIV-infected individuals and 20 HIV-uninfected controls were examined. Patients were classified as suboptimal responders, sIR (n = 10, CD4 T-cell <350 cells/ul) and optimal responders, oIR (n = 16, CD4 T-cell >500 cells/ul) after a minimum of 2 years on suppressive ART. Canonical correlation analysis(CCA) and multiple regression modelling were used to explore the association between fecal bacterial taxa abundance and immunological profiles in optimal and suboptimal responders. We found Fusobacterium was significantly enriched among the HIV-infected and the sIR group. CCA results showed that Fusobacterium abundance was negatively correlated with CD4 T-cell counts, but positively correlated with CD4 T-cell activation and CD4 Tregs. Multiple linear regression analysis adjusted for age, baseline CD4 T-cell count, antibiotic exposure and MSM status indicated that higher Fusobacterium relative abundance was independently associated with poorer CD4 T-cell recovery following ART. Enrichment of Fusobacterium was associated with reduced immune recovery and persistent immune dysfunction following ART. Modulating the abundance of this bacterial taxa in the gut may be a viable intervention to improve immune reconstitution in our setting.
    Matched MeSH terms: HIV Infections/immunology*
  16. Boettiger DC, Nguyen VK, Durier N, Bui HV, Heng Sim BL, Azwa I, et al.
    J Acquir Immune Defic Syndr, 2015 Feb 01;68(2):186-95.
    PMID: 25590271 DOI: 10.1097/QAI.0000000000000411
    BACKGROUND: Roughly 4% of the 1.25 million patients on antiretroviral therapy (ART) in Asia are using second-line therapy. To maximize patient benefit and regional resources, it is important to optimize the timing of second-line ART initiation and use the most effective compounds available.

    METHODS: HIV-positive patients enrolled in the TREAT Asia HIV Observational Database who had used second-line ART for ≥6 months were included. ART use and rates and predictors of second-line treatment failure were evaluated.

    RESULTS: There were 302 eligible patients. Most were male (76.5%) and exposed to HIV via heterosexual contact (71.5%). Median age at second-line initiation was 39.2 years, median CD4 cell count was 146 cells per cubic millimeter, and median HIV viral load was 16,224 copies per milliliter. Patients started second-line ART before 2007 (n = 105), 2007-2010 (n = 147) and after 2010 (n = 50). Ritonavir-boosted lopinavir and atazanavir accounted for the majority of protease inhibitor use after 2006. Median follow-up time on second-line therapy was 2.3 years. The rates of treatment failure and mortality per 100 patient/years were 8.8 (95% confidence interval: 7.1 to 10.9) and 1.1 (95% confidence interval: 0.6 to 1.9), respectively. Older age, high baseline viral load, and use of a protease inhibitor other than lopinavir or atazanavir were associated with a significantly shorter time to second-line failure.

    CONCLUSIONS: Increased access to viral load monitoring to facilitate early detection of first-line ART failure and subsequent treatment switch is important for maximizing the durability of second-line therapy in Asia. Although second-line ART is highly effective in the region, the reported rate of failure emphasizes the need for third-line ART in a small portion of patients.

    Matched MeSH terms: HIV Infections/immunology
  17. Ramesh Kumar MR, Arunagirinathan N, Srivani S, Dhanasezhian A, Vijaykanth N, Manikandan N, et al.
    Microb Drug Resist, 2017 Jul;23(5):602-608.
    PMID: 27854149 DOI: 10.1089/mdr.2016.0034
    The antibiotic, trimethoprim-sulfamethoxazole (TMP-SMX), is generally used for prophylaxis in HIV individuals to protect them from Pneumocystis jiroveci infection. Long-term use of TMP-SMX develops drug resistance among bacteria in HIV patients. The study was aimed to detect the TMP-SMX resistance genes among gram-negative bacteria from HIV patients. TMP-SMX-resistant isolates were detected by the Kirby-Bauer disc diffusion method. While TMP resistance genes such as dfrA1, dfrA5, dfrA7, and dfrA17 and SMX resistance genes such as sul1 and sul2 were detected by multiplex PCR, class 1 and class 2 integrons were detected by standard monoplex PCR. Of the 151 TMP-SMX-resistant bacterial isolates, 3 were positive for sul1 alone, 48 for sul2 alone, 11 for dfrA7 alone, 21 for sul1 and sul2, 1 for sul1 and dfrA7, 23 for sul2 and dfrA7, 2 for sul2 and dfrA5, 41 for sul1, sul2, and dfrA7, and 1 for sul2, dfrA5, and dfrA7. Of 60 TMP-SMX-resistant isolates positive for integrons, 44 had class 1 and 16 had class 2 integrons. It was found that the prevalence of sul genes (n = 202; p HIV patients in India. Therefore, this study indicates that dissemination of TMP-SMX resistance genes and class 1 and class 2 integrons along with β-lactamase production among gram-negative bacteria in HIV patients will certainly make their treatment to bacterial infections more complicated in clinical settings.
    Matched MeSH terms: HIV Infections/immunology
  18. Norazmi MN, Suarn S
    Immunol Lett, 1994 Dec;43(3):177-82.
    PMID: 7721330
    The CD4+ T-lymphocyte absolute count (CD4ac), CD4+ T-lymphocyte percentage (CD4%) and total lymphocyte count (Løac) were assessed in HIV-seropositive intravenous drug users (IVDU) with reference to their correlation with the clinical categories A, B, and C as stipulated by the Centre of Disease Control and Prevention, USA (CDC) and with each other. It was found that while the CD4ac and Løac correlated with the clinical categories, CD4% did not. This may suggest that in our local setting, the CD4% may not necessarily be a suitable alternative marker to CD4ac as proposed by CDC. Furthermore, the CD4% of the normal subjects in this study was found to be relatively lower than the reported Caucasian levels. This may indicate that the use of the cut-off level of less than 14% as an AIDS-defining criteria may not be applicable for our HIV-seropositive IVDU. In addition, unlike the CD4ac which correlated directly with CD4% and Løac, the CD4% did not correlate with Løac. Therefore, due to the observed disparity with clinical status of patients and its possibly lower levels in our normal population, CD4% as a marker for staging HIV disease should be used with caution in our setting. Such findings may also have an impact on the use of established markers for the monitoring and classification of HIV-infected individuals in this region.
    Matched MeSH terms: HIV Infections/immunology*
  19. Rothan HA, Bidokhti MRM, Byrareddy SN
    J Autoimmun, 2018 05;89:11-20.
    PMID: 29352633 DOI: 10.1016/j.jaut.2018.01.002
    Dissemination of vector-borne viruses, such as Zika virus (ZIKV), in tropical and sub-tropical regions has a complicated impact on the immunopathogenesis of other endemic viruses such as dengue virus (DENV), chikungunya virus (CHIKV) and human immunodeficiency virus (HIV). The consequences of the possible co-infections with these viruses have specifically shown significant impact on the treatment and vaccination strategies. ZIKV is a mosquito-borne flavivirus from African and Asian lineages that causes neurological complications in infected humans. Many of DENV and CHIKV endemic regions have been experiencing outbreaks of ZIKV infection. Intriguingly, the mosquitoes, Aedes Aegypti and Aedes Albopictus, can simultaneously transmit all the combinations of ZIKV, DENV, and CHIKV to the humans. The co-circulation of these viruses leads to a complicated immune response due to the pre-existence or co-existence of ZIKV infection with DENV and CHIKV infections. The non-vector transmission of ZIKV, especially, via sexual intercourse and placenta represents an additional burden that may hander the treatment strategies of other sexually transmitted diseases such as HIV. Collectively, ZIKV co-circulation and co-infection with other viruses have inevitable impact on the host immune response, diagnosis techniques, and vaccine development strategies for the control of these co-infections.
    Matched MeSH terms: HIV Infections/immunology
  20. Saeidi A, Chong YK, Yong YK, Tan HY, Barathan M, Rajarajeswaran J, et al.
    Cell Immunol, 2015 Sep;297(1):19-32.
    PMID: 26071876 DOI: 10.1016/j.cellimm.2015.05.005
    The role of T-cell immunosenescence and functional CD8(+) T-cell responses in HIV/TB co-infection is unclear. We examined and correlated surrogate markers of HIV disease progression with immune activation, immunosenescence and differentiation using T-cell pools of HIV/TB co-infected, HIV-infected and healthy controls. Our investigations showed increased plasma viremia and reduced CD4/CD8 T-cell ratio in HIV/TB co-infected subjects relative to HIV-infected, and also a closer association with changes in the expression of CD38, a cyclic ADP ribose hydrolase and CD57, which were consistently expressed on late-senescent CD8(+) T cells. Up-regulation of CD57 and CD38 were directly proportional to lack of co-stimulatory markers on CD8(+) T cells, besides diminished expression of CD127 (IL-7Rα) on CD57(+)CD4(+) T cells. Notably, intracellular IFN-γ, perforin and granzyme B levels in HIV-specific CD8(+) T cells of HIV/TB co-infected subjects were diminished. Intracellular CD57 levels in HIV gag p24-specific CD8(+) T cells were significantly increased in HIV/TB co-infection. We suggest that HIV-TB co-infection contributes to senescence associated with chronic immune activation, which could be due to functional insufficiency of CD8(+) T cells.
    Matched MeSH terms: HIV Infections/immunology*
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