Journal of AIDS & Clinical Research

Substantial progress in the understanding of HIV and CD4 cell dynamics using computational models undergirded by sound epidemiologic and mathematical principles has been achieved. The early stages of the applications of these models were based on relatively simple mathematical models that considered the body as a one-compartment system. In spite of these models attractiveness due to the experimental and/or mathematical standpoints, the underlying simplification neglected a lot of important factors affecting the population dynamics both on macro (human) and micro (cellular) population levels. This simplification also affected the kinetics linked to the immunology, infection and chemotherapy dynamics throughout the host. Epidemiologic research involves the study of a complex set of host, environmental and causative agent factors as they interact to impact health and diseases in any given population whether biotic or abiotic. This leads in generating large data sets which require the use of powerful computational methods for studying these large and complex models by means of computational epidemiologic methods. Another dimension of a great challenging problem to public health decision makers is that of emerging diseases, as they have to face and deal with a lot of uncertainty at the early stages of disease outbreaks. However, at this juncture, epidemiologic problem-solving and decision-making often proceeds in the face of uncertainties and limited information. One methodology to address these types of shortcomings is the application of risk analysis. Risk analysis is a process for decision making under uncertainty that consists of three fundamental tasks: risk management, risk assessment, and risk communication. Excitingly, the prospective role that computational models and risk analysis may possibly play in the advancement of the theoretical understanding of disease processes and the identification of specific intervention strategies holds the potential to impact and save human lives.

Background: Extant literature finds that 80% of HIV-infected patients present with otorhinolaryngological symptoms during the course of the infection. To date, no studies have defined HIV-associated ENT manifestations in Iran. To fill this gap in the literature, this study characterizes ENT signs and symptoms in HIV-infected individuals in Tehran, Iran.

Methods: The cross-sectional study consisted of 98 HIV infected patients who were referred to a Voluntary Counseling and Testing (VCT) center of Imam Khomeini hospital, Tehran from September 2007 to September 2008. A detailed history and physical examination was conducted for each patient. A questionnaire based on ENT manifestations was designed for the study. Para clinical assessments were carried out if any ENT manifestation was present. Analysis included calculations of mean values of quantitative associations between ENT symptoms and otological and nasopharyngeal complaints as well as ENT symptoms and demographic characteristics. Statistical analysis was estimated using either Chi-square test or t- test.

Results: Among ENT manifestations, otological and nasopharyngeal complaints were most common. Hearing loss (61%), post-nasal discharge (23.5%), xerostomia (39.8%) and voice change (23.5%) were the most frequently cited complaints by participants. In clinical examination, external otitis (6%), mucosal dryness of nasopharynx (6.1%), candidiasis (9.2%), posterior (7.1%) and anterior (6.1%) lymphadenopathies were also common findings. Lower CD4 count was associated with increased prevalence of oropharyngeal conditions. In addition, the duration of HIV infection was significantly associated with oropharyngeal conditions.

Conclusion: ENT evaluations are highly recommended for early diagnosis, especially in patients with specific symptoms in unusual locations.

Background: Little is known about HIV/Hepatitis C Virus (HCV) co-infection in resource-limited countries, although chronic HCV infection is one of the most relevant comorbidities in HIV population. The aim of this study was to determine the severity of liver disease in a cohort of HIV/HCV co-infected patients followed in Calmette Hospital, Phnom Penh, Cambodia, and to analyse the impact of HCV infection on antiretroviral therapy efficacy and hepatotoxicity.

Methods: HIV patients with positive HCV antibodies were enrolled in this cross-sectional study. HIV monoinfected patients formed the control group. Transverse evaluation of co-infected patients was performed collecting clinical, biological, virological and ultrasonographic data. HIV course, response to antiretroviral therapy and frequency of hepatocytolysis were compared in both groups.

Results: Among 50 HIV patients known with HCV antibodies, 31 (62%) had positive plasma HCV RNA and were included (58% men, median age 44 years). HCV genotype 1 was the most prevalent (68%), followed by genotype 6 (25%). Twelve patients (39%) met clinical, biological and/or ultrasonographic criteria for cirrhosis. FibroTest stage was 3-4 in 16 patients (52%). HIV/HCV co-infected patients demonstrated similar immune restoration and virological response to antiretroviral therapy as the 160 HIV mono-infected patients. Co-infected patients were more likely to have alanine aminotransferase elevation at baseline and to develop grade 2 or 3 hepatocytolysis in the two years after antiretroviral therapy initiation, specifically when nevirapine was used during the first six months of treatment.

Conclusions: HIV/HCV co-infected patients are at increased risk for acquiring severe hepatic fibrosis. HCV coinfection does not affect response to ART. Efavirenz should be preferred to nevirapine in co-infected patients due to hepatotoxicity. Further research is required to target access to appropriate management of HIV/HCV co-infections in resource-limited countries.

Objective: Disparities in anal cancer incidence among Hawaii’s HIV-infected minority population is an emerging health concern. Although anal cytology/anoscopy are effective anal cancer screening tools, social barriers exist that prevent individuals from seeking appropriate care. Design: Community based participatory research (CBPR) principles were applied to develop resources, including testing a self-obtained anal specimen procedure, to increase anal cancer screening among Hawaii’s underserved/ minority populations.

Methods: A team of community members, academic researchers, and health care providers developed culturally-sensitive educational/recruitment materials regarding anal cancer risk targeting underserved/minority HIVinfected individuals. Self- and health care provider (HCP)-obtained anal cancer screening specimens were reviewed for cytology and tested for human papillomavirus DNA. A follow-up evaluation elicited feedback on attitudes and experiences.

Results: Community discussion sessions identified key messages about anal cancer, anal cancer screening, and HPV infection for materials and were used, that successfully recruited 46 individuals (38 males/8 females; 9 Native Hawaiians/Pacific Islanders/Asians, 2 Blacks, 6 Hispanics, 6 American Indian/Alaskan Natives, 23 Whites). Concordance in cytology results between self- and HCP-obtained specimens was moderated (kappa=0.37) with the perception that the self-obtained specimen procedure was private (93%), safe (100%), and easy to manage (100%); and a majority (92%) willing to use the self-obtained method again.

Conclusions: CBPR was a practical approach in engaging Hawaii’s HIV-infected minority participation in anal cancer screening research. Community outreach and recruitment efforts suggested that self-obtained screening specimens could be an acceptable and effective means to reach Hawaii’s HIV-infected ethnic minorities.

Background: Human immunodeficiency virus/acquired immunodeficiency disease syndrome-associated mortality contributes considerably to overall mortality rates among adults in the United States. The purpose of this review is to systematically examine conceptual approaches that have been used to evaluate the association between socioeconomic status of people infected with human immunodeficiency virus and their survival and summarize existing evidence regarding the association between socioeconomic status and mortality due to human immunodeficiency virus/acquired immunodeficiency disease syndrome.

Methods: We systematically retrieved neighborhood and individual-level studies of acquired immunodeficiency disease syndrome-related or all-cause mortality among patients diagnosed with human immunodeficiency virus that reported original data and analyzed socioeconomic status as a predictor of mortality.

Results: We included 21 studies (19 cohort and 2 case-control studies). Heterogeneity in both the conceptual approaches to socioeconomic status measurements and selection of variables for the adjustment of the measure of association precluded meta-analysis of the results. Six studies observing populations before the introduction of highly active antiretroviral therapy found that socioeconomic status was not associated with human immunodeficiency virus/acquired immunodeficiency disease syndrome mortality. In the post- highly active antiretroviral therapy period socioeconomic status was inconsistently associated with Human immunodeficiency virus/acquired immunodeficiency disease syndrome mortality risk in studies adjusting for highly active antiretroviral therapy use.

Conclusion: Further studies considering multilevel socioeconomic status measurements and controlling for treatment and clinical variables are needed to enhance understanding of the role of socioeconomic gradients on human immunodeficiency virus outcomes.

Although HIV and antiretroviral therapy (ART) have been linked with an increased cardiovascular risk, the pathological pathways remain unknown. We assessed whether secretory phospholipase A2 (sPLA2), high-sensitivity C-reactive protein (hs-CRP), vascular cell adhesion molecule (VCAM), thiobarbituric acid reactive species (TBARS), Superoxide dismutases (SOD), adiponectin and resistin were elevated in HIV infected patients with detectable and undetectable viral load compared to a control group matched for age, sex and cardiovascular risk factors. We evaluated its correlation with traditional and no traditional cardiovascular risk factors and carotid intima-media thickness. Levels of sPLA2 (median [IQR]) were 8.35 (5.36, 9.6) pg/ml, hsCRP were 3.3 (IQR, 1.27, 5.28) mg/L, VCAM 945.6 (IQR, 655.9, 1404.05) ng/ml and TBARS 1.69 (IQR, 1.39, 1.97) uM/L in HIV infected group compared to levels of sPLA2 1.22 (IQR, 0.69, 2.62) pg/ml (p<0.001), hsCRP 3.05 (IQR, 2.68, 3.27) mg/L (p=0.05), VCAM 678.35 (IQR, 530.39, 831.04) ng/ml (p<0.001) and TBARS 7.47 (IQR, 5.03, 10.4) uM/L (p<0.001) in control group. Levels of VCAM (median [IQR]) were 1047.19 (IQR, 609.06, 1084.1) ng/ml (p=0.015) and sPLA2 were 7.6 (IQR, 5.25, 9.6) pg/ml (p<0.001) in HIV infected patients with undetectable viral load compared to control group. There was a good correlation between all analyzed biomarkers and cardiovascular risk factors. In conclusion, HIV infection induces chronic inflammation and endothelial activation that is not completely suppressed by the treatment.