Members of the Australasian Society for HIV Medicine (ASHM) include doctors, scientists, social scientists, epidemiologists, nurses and other allied health professionals who work in the field of HIV medicine, and the annual ASHM conference is targeted towards this membership. Furthermore, the ASHM has strong partnerships across the Asia and Pacific regions and, therefore, doctors, social researchers, nongovernment organizations and groups representing people living with HIV/AIDS from countries from the Asia and Pacific regions were well represented. The conference was jointly funded by the Australian Government, Queensland and Western Australia State Health Departments and the pharmaceutical industry, and was organized around four themes: understanding and identifying HIV: basic science, biology and pathogenesis; managing HIV: clinical management and the the experience of living with HIV; preventing HIV; and HIV in populations.
{"title":"Australasian HIV/AIDS Conference 2009","authors":"E. Wright, P. Cameron, E. Reis, S. Lewin","doi":"10.2217/HIV.09.59","DOIUrl":"https://doi.org/10.2217/HIV.09.59","url":null,"abstract":"Members of the Australasian Society for HIV Medicine (ASHM) include doctors, scientists, social scientists, epidemiologists, nurses and other allied health professionals who work in the field of HIV medicine, and the annual ASHM conference is targeted towards this membership. Furthermore, the ASHM has strong partnerships across the Asia and Pacific regions and, therefore, doctors, social researchers, nongovernment organizations and groups representing people living with HIV/AIDS from countries from the Asia and Pacific regions were well represented. The conference was jointly funded by the Australian Government, Queensland and Western Australia State Health Departments and the pharmaceutical industry, and was organized around four themes: understanding and identifying HIV: basic science, biology and pathogenesis; managing HIV: clinical management and the the experience of living with HIV; preventing HIV; and HIV in populations.","PeriodicalId":88510,"journal":{"name":"HIV therapy","volume":"29 1","pages":"9-11"},"PeriodicalIF":0.0,"publicationDate":"2010-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74462630","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Post-translational modifications occur on an array of proteins in a majority of organisms. These modifications range from the addition of small biomolecules to large sugar moieties and induce functional and/or structural alterations that extend the functional repertoire of proteins. While the importance of phosphorylation in key cellular events is now widely accepted, less is known about the effects of protein methylation. This review focuses on the post-translational modification, protein methylation and, in particular, the role of protein arginine methylation. Recent findings of the role arginine methylation plays in HIV-1 replication, other viral diseases and a wide range of human diseases are summarized. We explore how elucidating this important cellular mechanism, can lead to an improved understanding of HIV-1, viral illnesses and other human diseases. Finally, we discuss the potential of protein arginine methylation as a worthwhile novel therapeutic target in the combat against a range of viral infe...
{"title":"Protein arginine methylation: a pivotal factor and a target for novel HIV-therapeutics, other viruses and multiple diseases","authors":"L. Mirto, S. Piller","doi":"10.2217/HIV.09.56","DOIUrl":"https://doi.org/10.2217/HIV.09.56","url":null,"abstract":"Post-translational modifications occur on an array of proteins in a majority of organisms. These modifications range from the addition of small biomolecules to large sugar moieties and induce functional and/or structural alterations that extend the functional repertoire of proteins. While the importance of phosphorylation in key cellular events is now widely accepted, less is known about the effects of protein methylation. This review focuses on the post-translational modification, protein methylation and, in particular, the role of protein arginine methylation. Recent findings of the role arginine methylation plays in HIV-1 replication, other viral diseases and a wide range of human diseases are summarized. We explore how elucidating this important cellular mechanism, can lead to an improved understanding of HIV-1, viral illnesses and other human diseases. Finally, we discuss the potential of protein arginine methylation as a worthwhile novel therapeutic target in the combat against a range of viral infe...","PeriodicalId":88510,"journal":{"name":"HIV therapy","volume":"40 1","pages":"65-81"},"PeriodicalIF":0.0,"publicationDate":"2010-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90220149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Millions of HIV-infected individuals are at risk to yellow fever (YF), a severe hemorrhagic disease, which is endemic in tropical areas of Africa and Latin America. The 17D YF vaccine (17DV) is the most effective preventive strategy. Increased vaccine coverage campaigns guided by the WHO, try to prevent outbreaks in YF-endemic countries, including HIV-endemic areas. Data regarding safety and immunogenicity of 17DV in HIV-infected individuals are limited to small studies, mainly in travelers with CD4 cell counts above 200 cells/mm3, demonstrating a reduced immune response and good tolerability. However, rare serious adverse events cannot be excluded. According to current recommendations, 17DV should only be given to asymptomatic HIV-infected individuals with a CD4 cell count above 200 cell/mm3. Data concerning 17DV in HIV-infected individuals living in YF-endemic areas are missing, making mass immunization campaigns against YF very challenging. There is a special need for further studies to investigate the...
{"title":"Yellow fever vaccination in HIV‑infected patients","authors":"O. Veit, C. Hatz, M. Niedrig, H. Furrer","doi":"10.2217/HIV.09.52","DOIUrl":"https://doi.org/10.2217/HIV.09.52","url":null,"abstract":"Millions of HIV-infected individuals are at risk to yellow fever (YF), a severe hemorrhagic disease, which is endemic in tropical areas of Africa and Latin America. The 17D YF vaccine (17DV) is the most effective preventive strategy. Increased vaccine coverage campaigns guided by the WHO, try to prevent outbreaks in YF-endemic countries, including HIV-endemic areas. Data regarding safety and immunogenicity of 17DV in HIV-infected individuals are limited to small studies, mainly in travelers with CD4 cell counts above 200 cells/mm3, demonstrating a reduced immune response and good tolerability. However, rare serious adverse events cannot be excluded. According to current recommendations, 17DV should only be given to asymptomatic HIV-infected individuals with a CD4 cell count above 200 cell/mm3. Data concerning 17DV in HIV-infected individuals living in YF-endemic areas are missing, making mass immunization campaigns against YF very challenging. There is a special need for further studies to investigate the...","PeriodicalId":88510,"journal":{"name":"HIV therapy","volume":"25 1","pages":"17-26"},"PeriodicalIF":0.0,"publicationDate":"2010-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78871320","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
More than 25 years after the discovery of HIV and despite several vaccine trials, the correlates of immune protection are still not identified. Successful vaccine strategies will likely involve induction of both humoral and cellular immunity in order to prevent or limit HIV infection and to stimulate protective immune responses in HIV-infected individuals. The major difficulties in this quest include the various mechanisms of immune escape developed by HIV and the fact that not all immune responses against HIV have strong antiviral functions. This article will focus on an underestimated aspect of any T-cell-based arm of vaccine strategies: the mechanisms of epitope processing and its contribution to the pattern of HIV-specific CD8+ T-cell responses. This article will also present current complementary research approaches towards the identification of CD8+ T-cell protective immune responses and the design of immunogens aimed at selectively inducing CD8+ T-cell protective immune responses against HIV, one o...
{"title":"MHC-I-restricted HIV epitope processing, immune control and immunogen design","authors":"S. Gall","doi":"10.2217/HIV.09.57","DOIUrl":"https://doi.org/10.2217/HIV.09.57","url":null,"abstract":"More than 25 years after the discovery of HIV and despite several vaccine trials, the correlates of immune protection are still not identified. Successful vaccine strategies will likely involve induction of both humoral and cellular immunity in order to prevent or limit HIV infection and to stimulate protective immune responses in HIV-infected individuals. The major difficulties in this quest include the various mechanisms of immune escape developed by HIV and the fact that not all immune responses against HIV have strong antiviral functions. This article will focus on an underestimated aspect of any T-cell-based arm of vaccine strategies: the mechanisms of epitope processing and its contribution to the pattern of HIV-specific CD8+ T-cell responses. This article will also present current complementary research approaches towards the identification of CD8+ T-cell protective immune responses and the design of immunogens aimed at selectively inducing CD8+ T-cell protective immune responses against HIV, one o...","PeriodicalId":88510,"journal":{"name":"HIV therapy","volume":"18 1","pages":"101-117"},"PeriodicalIF":0.0,"publicationDate":"2010-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90449161","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Early in the AIDS epidemic opportunistic lung infections, most notably Pneumocystis infection, dominated the clinical picture and were the most common cause of death in HIV-infected individuals. With the progressive development of effective antiretroviral treatments and prophylaxis against Pneumocystis, the prognosis in HIV/AIDS has improved dramatically with median survival now greater than a decade. However, lung infections from opportunistic, as well as typical bacterial pathogens remain a major cause of morbidity and are still the leading cause of death from HIV/AIDS. In addition, as the survival of infected individuals has increased, it is becoming apparent that other more-chronic lung diseases, including emphysema and cancer, are more common in these individuals. Although the mechanisms by which HIV/AIDS increases the risk of both infectious and noninfectious lung diseases are still being investigated, there is emerging evidence from clinical and experimental studies that HIV causes oxidant stress w...
{"title":"Obstructive lung disease and HIV/AIDS in the HAART era.","authors":"A. Morris, D. Guidot","doi":"10.2217/HIV.09.53","DOIUrl":"https://doi.org/10.2217/HIV.09.53","url":null,"abstract":"Early in the AIDS epidemic opportunistic lung infections, most notably Pneumocystis infection, dominated the clinical picture and were the most common cause of death in HIV-infected individuals. With the progressive development of effective antiretroviral treatments and prophylaxis against Pneumocystis, the prognosis in HIV/AIDS has improved dramatically with median survival now greater than a decade. However, lung infections from opportunistic, as well as typical bacterial pathogens remain a major cause of morbidity and are still the leading cause of death from HIV/AIDS. In addition, as the survival of infected individuals has increased, it is becoming apparent that other more-chronic lung diseases, including emphysema and cancer, are more common in these individuals. Although the mechanisms by which HIV/AIDS increases the risk of both infectious and noninfectious lung diseases are still being investigated, there is emerging evidence from clinical and experimental studies that HIV causes oxidant stress w...","PeriodicalId":88510,"journal":{"name":"HIV therapy","volume":"31 1","pages":"41-54"},"PeriodicalIF":0.0,"publicationDate":"2010-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72938503","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Since AIDS emerged almost three decades ago, there have been considerable advances in the field of antiretroviral chemotherapy for those chronically infected with HIV-1. However, this therapy is noncurative and as our understanding of HIV-1 immunopathogenesis increases, it is becoming apparent that further therapeutic interventions are required to reverse the devastating effects of HIV-1 infection worldwide. While viral clearance remains the principle goal of HIV-1 treatment, this article describes immunotherapeutic options that target the immunological effects of the virus, to reduce its presence in the body and counteract viral-induced T-cell dysfunction and inhibition. Such approaches may augment existing antiretroviral therapy to overturn virus-induced T-cell anergy in the infected host, improving levels of immune control that reduce viremia and decrease the rate of transmission.
{"title":"T-cell dysfunction in HIV-1 infection: targeting the inhibitors","authors":"J. Downey, N. Imami","doi":"10.2217/HIV.09.51","DOIUrl":"https://doi.org/10.2217/HIV.09.51","url":null,"abstract":"Since AIDS emerged almost three decades ago, there have been considerable advances in the field of antiretroviral chemotherapy for those chronically infected with HIV-1. However, this therapy is noncurative and as our understanding of HIV-1 immunopathogenesis increases, it is becoming apparent that further therapeutic interventions are required to reverse the devastating effects of HIV-1 infection worldwide. While viral clearance remains the principle goal of HIV-1 treatment, this article describes immunotherapeutic options that target the immunological effects of the virus, to reduce its presence in the body and counteract viral-induced T-cell dysfunction and inhibition. Such approaches may augment existing antiretroviral therapy to overturn virus-induced T-cell anergy in the infected host, improving levels of immune control that reduce viremia and decrease the rate of transmission.","PeriodicalId":88510,"journal":{"name":"HIV therapy","volume":"120 1","pages":"83-99"},"PeriodicalIF":0.0,"publicationDate":"2010-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89827718","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
J. Hoffman, J. Griensven, R. Colebunders, Mehri McKellar
As a result of successful antiretroviral treatment over the last 20 years, HIV has become more of a chronic disease for practitioners to manage, requiring careful, but routine, clinical monitoring. Laboratory markers, such as the HIV-1 RNA viral load and CD4 cell count, are regularly used for patient management in addition to predicting disease progression and/or treatment outcomes. The HIV viral load is considered to be the gold standard for evaluating treatment success, although it is often limited by the cost. Furthermore, in certain cases, there is a mismatch between an undetectable viral load (<50 copies/ml) and the absence of immune reconstitution, which can be confusing to both the treatment provider and patient. In this review, the utility of the CD4 count as a predictor for HIV disease progression in patients not on therapy is evaluated, as well as a method for monitoring a patient’s response to therapy. Its use in predicting immune reconstitution in patients initiating antiretrovirals is also id...
{"title":"Role of the CD4 count in HIV management","authors":"J. Hoffman, J. Griensven, R. Colebunders, Mehri McKellar","doi":"10.2217/HIV.09.58","DOIUrl":"https://doi.org/10.2217/HIV.09.58","url":null,"abstract":"As a result of successful antiretroviral treatment over the last 20 years, HIV has become more of a chronic disease for practitioners to manage, requiring careful, but routine, clinical monitoring. Laboratory markers, such as the HIV-1 RNA viral load and CD4 cell count, are regularly used for patient management in addition to predicting disease progression and/or treatment outcomes. The HIV viral load is considered to be the gold standard for evaluating treatment success, although it is often limited by the cost. Furthermore, in certain cases, there is a mismatch between an undetectable viral load (<50 copies/ml) and the absence of immune reconstitution, which can be confusing to both the treatment provider and patient. In this review, the utility of the CD4 count as a predictor for HIV disease progression in patients not on therapy is evaluated, as well as a method for monitoring a patient’s response to therapy. Its use in predicting immune reconstitution in patients initiating antiretrovirals is also id...","PeriodicalId":88510,"journal":{"name":"HIV therapy","volume":"40 1","pages":"27-39"},"PeriodicalIF":0.0,"publicationDate":"2010-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84466178","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Evaluation of: Holden LG, Prochnow C, Chang YP et al.: Crystal structure of the anti-viral APOBEC3G catalytic domain and functional implications. Nature 456(7218), 121–124 (2008). APOBEC3 proteins belong to a family of cytidine deaminases that can inhibit a variety of retroviruses as well as a range of endogenous retroelements. In particular, APOBEC3G can strongly restrict HIV-1 Vif deletion mutants. Normally, however, HIV-1 counters this restriction by using the viral protein Vif to direct the degradation of APOBEC3 proteins by targeting them for proteasomal degradation. However, in the absence of Vif, APOBEC3G can be packaged into virions and, upon re-infection of new cells, can induce C-to-U mutations in the newly reverse-transcribed, ssDNA. Understanding the structural elements of APOBEC3 proteins, their mechanism of action and how they interact with proteins such as HIV-1 Vif, is crucial for intelligent drug design. In this recently published manuscript, the crystal structure of the C-terminal deamin...
{"title":"Crystal structure of the C-terminal deaminase domain of APOBEC3G: implications and projections","authors":"A. Niewiadomska, X. Yu","doi":"10.2217/17584310.3.1.31","DOIUrl":"https://doi.org/10.2217/17584310.3.1.31","url":null,"abstract":"Evaluation of: Holden LG, Prochnow C, Chang YP et al.: Crystal structure of the anti-viral APOBEC3G catalytic domain and functional implications. Nature 456(7218), 121–124 (2008). APOBEC3 proteins belong to a family of cytidine deaminases that can inhibit a variety of retroviruses as well as a range of endogenous retroelements. In particular, APOBEC3G can strongly restrict HIV-1 Vif deletion mutants. Normally, however, HIV-1 counters this restriction by using the viral protein Vif to direct the degradation of APOBEC3 proteins by targeting them for proteasomal degradation. However, in the absence of Vif, APOBEC3G can be packaged into virions and, upon re-infection of new cells, can induce C-to-U mutations in the newly reverse-transcribed, ssDNA. Understanding the structural elements of APOBEC3 proteins, their mechanism of action and how they interact with proteins such as HIV-1 Vif, is crucial for intelligent drug design. In this recently published manuscript, the crystal structure of the C-terminal deamin...","PeriodicalId":88510,"journal":{"name":"HIV therapy","volume":"12 1","pages":"31-34"},"PeriodicalIF":0.0,"publicationDate":"2009-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82391044","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Resistance to antiviral therapy is the limiting factor in the successful management of HIV. In general, the K65R mutation is rarely selected (1.7-4%) with tenofovir disoproxil fumarate (TDF), abacavir (ABC), didanosine (ddI), and stavudine (d4T), as compared with the high incidence (>40%) of thymidine analog mutations associated with zidovudine and d4T. The high barrier to the development of K65R may reflect a combination of factors, including the high potency of K65R-selecting drugs, including recommended TDF/emtricitabine and ABC/lamivudine (ABC/3TC) combinations; the partial (low-intermediate level) profile of cross-resistance conferred by K65R to TDF, ABC and 3TC; the favorable viral fitness constraint imposed by K65R and the 3TC/emtricitabine-associated M184V mutations; the bidirectional antagonism between the K65R and thymidine analog mutation pathways; and unique RNA structural considerations in the region surrounding codon 65. Nevertheless, surprisingly high levels of treatment failures and K65R resistance may be associated with triple nucleoside analog regimens. The use of TDF + ABC, TDF + ddI and ABC + d4T in combination with 3TC or emtricitabine should be avoided. This selection of K65R may be reduced by the inclusion of zidovudine in two-four nucleoside reverse-transcriptase regimens. Clinical studies have demonstrated an increased frequency of K65R in association with suboptimal d4T and ddI regimens, as well as nevirapine and its resistance mutations Y181C and G190A. The potential for the development of the K65R mutation in subtype C is particularly problematic wherein a signature KKK nucleotide motif, at codons 64, 65 and 66 in reverse transcriptase, appear to lead to template pausing, facilitating the selection of K65R. Optimizing regimens may attenuate the emergence of K65R, leading to better long-term treatment management in different geographic settings. TDF-based regimens are the leading candidates for first- and second-line therapy, microbicides and chemoprophylaxis strategies.
{"title":"The K65R mutation in HIV-1 reverse transcriptase: genetic barriers, resistance profile and clinical implications.","authors":"Bluma G Brenner, Dimitrios Coutsinos","doi":"10.2217/hiv.09.40","DOIUrl":"https://doi.org/10.2217/hiv.09.40","url":null,"abstract":"<p><p>Resistance to antiviral therapy is the limiting factor in the successful management of HIV. In general, the K65R mutation is rarely selected (1.7-4%) with tenofovir disoproxil fumarate (TDF), abacavir (ABC), didanosine (ddI), and stavudine (d4T), as compared with the high incidence (>40%) of thymidine analog mutations associated with zidovudine and d4T. The high barrier to the development of K65R may reflect a combination of factors, including the high potency of K65R-selecting drugs, including recommended TDF/emtricitabine and ABC/lamivudine (ABC/3TC) combinations; the partial (low-intermediate level) profile of cross-resistance conferred by K65R to TDF, ABC and 3TC; the favorable viral fitness constraint imposed by K65R and the 3TC/emtricitabine-associated M184V mutations; the bidirectional antagonism between the K65R and thymidine analog mutation pathways; and unique RNA structural considerations in the region surrounding codon 65. Nevertheless, surprisingly high levels of treatment failures and K65R resistance may be associated with triple nucleoside analog regimens. The use of TDF + ABC, TDF + ddI and ABC + d4T in combination with 3TC or emtricitabine should be avoided. This selection of K65R may be reduced by the inclusion of zidovudine in two-four nucleoside reverse-transcriptase regimens. Clinical studies have demonstrated an increased frequency of K65R in association with suboptimal d4T and ddI regimens, as well as nevirapine and its resistance mutations Y181C and G190A. The potential for the development of the K65R mutation in subtype C is particularly problematic wherein a signature KKK nucleotide motif, at codons 64, 65 and 66 in reverse transcriptase, appear to lead to template pausing, facilitating the selection of K65R. Optimizing regimens may attenuate the emergence of K65R, leading to better long-term treatment management in different geographic settings. TDF-based regimens are the leading candidates for first- and second-line therapy, microbicides and chemoprophylaxis strategies.</p>","PeriodicalId":88510,"journal":{"name":"HIV therapy","volume":"3 6","pages":"583-594"},"PeriodicalIF":0.0,"publicationDate":"2009-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2217/hiv.09.40","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28744945","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
HIV is a significant cause of severe acute malnutrition (SAM) in Africa, which radically alters its epidemiology and clinical presentation. Clinical diagnosis of HIV is difficult: marasmus, oral candidiasis and persistent diarrhea are associated with HIV, but are also commonly observed in SAM. The same pathogens have been identified in HIV-infected and -uninfected children with SAM, but the former respond less well to treatment. HIV also affects children’s nutrition through food insecurity and infant feeding practice. A threefold greater mortality (30%) occurs in children living with HIV during nutrition program admission and continues after discharge. Nutrition interventions alone are able to achieve a nutritional cure in most HIV-infected children, including those with severe immunodeficiency, although weight gain is slower. Nonresponse to nutritional therapy is a defining WHO clinical criteria for initiating antiretroviral treatment, and malnutrition is the strongest predictor of death after starting a...
{"title":"Severe acute malnutrition and HIV in African children.","authors":"J. Bunn","doi":"10.2217/HIV.09.43","DOIUrl":"https://doi.org/10.2217/HIV.09.43","url":null,"abstract":"HIV is a significant cause of severe acute malnutrition (SAM) in Africa, which radically alters its epidemiology and clinical presentation. Clinical diagnosis of HIV is difficult: marasmus, oral candidiasis and persistent diarrhea are associated with HIV, but are also commonly observed in SAM. The same pathogens have been identified in HIV-infected and -uninfected children with SAM, but the former respond less well to treatment. HIV also affects children’s nutrition through food insecurity and infant feeding practice. A threefold greater mortality (30%) occurs in children living with HIV during nutrition program admission and continues after discharge. Nutrition interventions alone are able to achieve a nutritional cure in most HIV-infected children, including those with severe immunodeficiency, although weight gain is slower. Nonresponse to nutritional therapy is a defining WHO clinical criteria for initiating antiretroviral treatment, and malnutrition is the strongest predictor of death after starting a...","PeriodicalId":88510,"journal":{"name":"HIV therapy","volume":"283 1","pages":"595-611"},"PeriodicalIF":0.0,"publicationDate":"2009-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77059294","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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