Late presentation to HIV/AIDS care in Brazil among men who self-identify as heterosexual

ABSTRACT OBJECTIVE To analyze the factors associated with late presentation to HIV/AIDS services among heterosexual men. METHODS Men infected by HIV who self-identified as heterosexual (n = 543) were included in the study. Descriptive, biivariate and logistic regression analyses were performed to evaluate the factors associated with late presentation (defined as individuals whose first CD4 count was <350 cells/mm3) in the study population. RESULTS The prevalence of late presentation was 69.8%. The multivariate logistic analysis showed testing initiated by the provider (ORadjusted 3.75; 95%CI 2.45–5.63) increased the odds of late presentation. History of drug use (ORadjusted 0.59; 95%CI 0.38–0.91), history of having sexually transmitted infections (ORadjusted 0.64; 95%CI 0.42–0.97), and having less education (ORadjusted 0.63; 95%CI 0.41–0.97) were associated with a decreased odds of LP. CONCLUSIONS Provider initiated testing was the only variable to increase the odds of late presentation. Since the patients in this sample all self-identified as heterosexual, it appears that providers are not requesting they be tested for HIV until the patients are already presenting symptoms of AIDS. The high prevalence of late presentation provides additional evidence to shift towards routine testing and linkage to care, rather than risk-based strategies that may not effectively or efficiently engage individuals infected with HIV

Deep sequencing of hepatitis C virus reveals genetic compartmentalization in cerebrospinal fluid from cognitively impaired patients

Hepatitis C virus (HCV) causes neuropsychiatric impairment and fatigue with recent studies suggesting HCV invasion of the central nervous system (CNS). Our previous finding that endothelial cells from the blood-brain barrier support HCV infection warrants further investigation to elucidate whether the CNS can serve as a reservoir for independent HCV evolution.Cerebrospinal fluid (CSF) and plasma from six HCV-infected patients without liver disease or co-morbidities together with plasma from six healthy subjects were profiled for markers of immune activation and viral quasispecies measured by deep sequencing. Unsupervised data analyses were used to identify any associations between cytokine activation markers and clinical outcomes.Four of six HCV-infected patients showed significant evidence of cognitive dysfunction and fatigue. Deep sequencing revealed independent viral evolution within the CNS of two cognitively impaired patients. Principal component analysis of peripheral cytokines demonstrated that individuals without cognitive impairment clustered together while a distinct cytokine pattern emerged with patients exhibiting cognitive dysfunction and fatigue.Deep sequencing demonstrated unique viral variants in the CSF of two cognitively impaired patients consistent with CNS replication or sequestration. Meanwhile, compartmentalization was absent in infected patients with no neurocognitive impairment. Examination of cytokine profiles in HCV-infected patients with cognitive dysfunction revealed elevated peripheral cytokine levels resulting in a distinct cytokine profile that may be related to cognitive impairment or viral penetration into the CNS. Further studies to determine the significance of unique HCV variants within the CNS are warranted

Deep sequencing of hepatitis C virus reveals genetic compartmentalization in cerebrospinal fluid from cognitively impaired patients

Hepatitis C virus (HCV) causes neuropsychiatric impairment and fatigue with recent studies suggesting HCV invasion of the central nervous system (CNS). Our previous finding that endothelial cells from the blood-brain barrier support HCV infection warrants further investigation to elucidate whether the CNS can serve as a reservoir for independent HCV evolution.Cerebrospinal fluid (CSF) and plasma from six HCV-infected patients without liver disease or co-morbidities together with plasma from six healthy subjects were profiled for markers of immune activation and viral quasispecies measured by deep sequencing. Unsupervised data analyses were used to identify any associations between cytokine activation markers and clinical outcomes.Four of six HCV-infected patients showed significant evidence of cognitive dysfunction and fatigue. Deep sequencing revealed independent viral evolution within the CNS of two cognitively impaired patients. Principal component analysis of peripheral cytokines demonstrated that individuals without cognitive impairment clustered together while a distinct cytokine pattern emerged with patients exhibiting cognitive dysfunction and fatigue.Deep sequencing demonstrated unique viral variants in the CSF of two cognitively impaired patients consistent with CNS replication or sequestration. Meanwhile, compartmentalization was absent in infected patients with no neurocognitive impairment. Examination of cytokine profiles in HCV-infected patients with cognitive dysfunction revealed elevated peripheral cytokine levels resulting in a distinct cytokine profile that may be related to cognitive impairment or viral penetration into the CNS. Further studies to determine the significance of unique HCV variants within the CNS are warranted