Age at autism spectrum disorder diagnosis and its association with child and family characteristics in a tertiary care hospital in Malaysia.

Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder. Despite the absence of a cure, early diagnosis and intensive early intervention can improve the outcomes. However, little is known about the median age at ASD diagnosis in Malaysia or the child/family characteristics associated with early diagnosis. Therefore, this study aimed to determine the median age at ASD diagnosis among Malaysian children presenting to the country's largest public tertiary neurodevelopmental center and to investigate the possible demographic, child, and family characteristics associated with an early age at diagnosis. Data were collected between February 2017 and February 2019 from a database maintained by the child development unit of the country's largest publicly funded tertiary hospital, containing data from an ethnically diverse population. Among Malaysian children attending the clinic, the median age at ASD diagnosis was 48 months. Early autism diagnosis (<36 months of age) was associated with increased severity of social communication and interaction impairments, coexisting intellectual impairment, children from high socioeconomic status families, and children who receive joint care from their families and a maid or babysitter. The study findings highlight the socioeconomic inequalities in the country, a lack of parental awareness of early ASD signs, and the presence of cultural influences on the age at diagnosis of ASD.

Markers of Tissue Repair and Cellular Aging Are Increased in the Liver Tissue of Patients With HIV Infection Regardless of Presence of HCV Coinfection.

Liver disease is a leading cause of HIV-related mortality. Hepatitis C virus (HCV)-related fibrogenesis is accelerated in the setting of HIV coinfection, yet the mechanisms underlying this aggressive pathogenesis are unclear. We identified formalin-fixed paraffin-embedded liver tissue for HIV-infected patients, HCV-infected patients, HIV/HCV-coinfected patients, and controls at Duke University Medical Center. De-identified sections were stained for markers against the wound repair Hedgehog (Hh) pathway, resident T-lymphocytes, and immune activation and cellular aging. HIV infection was independently associated with Hh activation and markers of immune dysregulation in the liver tissue.

HIV-1 specific IgA detected in vaginal secretions of HIV uninfected women participating in a microbicide trial in Southern Africa are primarily directed toward gp120 and gp140 specificities.

BACKGROUND: Many participants in microbicide trials remain uninfected despite ongoing exposure to HIV-1. Determining the emergence and nature of mucosal HIV-specific immune responses in such women is important, since these responses may contribute to protection and could provide insight for the rational design of HIV-1 vaccines. METHODS AND FINDINGS: We first conducted a pilot study to compare three sampling devices (Dacron swabs, flocked nylon swabs and Merocel sponges) for detection of HIV-1-specific IgG and IgA antibodies in vaginal secretions. IgG antibodies from HIV-1-positive women reacted broadly across the full panel of eight HIV-1 envelope (Env) antigens tested, whereas IgA antibodies only reacted to the gp41 subunit. No Env-reactive antibodies were detected in the HIV-negative women. The three sampling devices yielded equal HIV-1-specific antibody titers, as well as total IgG and IgA concentrations. We then tested vaginal Dacron swabs archived from 57 HIV seronegative women who participated in a microbicide efficacy trial in Southern Africa (HPTN 035). We detected vaginal IgA antibodies directed at HIV-1 Env gp120/gp140 in six of these women, and at gp41 in another three women, but did not detect Env-specific IgG antibodies in any women. CONCLUSION: Vaginal secretions of HIV-1 infected women contained IgG reactivity to a broad range of Env antigens and IgA reactivity to gp41. In contrast, Env-binding antibodies in the vaginal secretions of HIV-1 uninfected women participating in the microbicide trial were restricted to the IgA subtype and were mostly directed at HIV-1 gp120/gp140.