Adaptation of Metabolomics and Microbiomic Research Protocols During the COVID-19 Pandemic.

Background: When the COVID-19 pandemic hit in 2020, researchers in the P30 Center for the Study of Symptom Science, Metabolomics, and Multiple Chronic Conditions at Emory University's Nell Hodgson Woodruff School of Nursing faced major challenges in recruitment and data collection because of limited access to the clinic and community facilities and the risk of COVID-19 exposure associated with in-person study contact.

Objectives: The purpose of this article is to (a) describe how a cadre of pilot/supplement principal investigators adapted their studies to allow for safe and trustworthy data collection during the COVID-19 pandemic (March 2020 through date of publication) and (b) discuss steps that facilitated the technical aspects of remote data collection, especially involving biological specimens.

Results: Four pilot studies and two administrative supplements within the center-all at different stages of execution-adopted various alternative remote recruitment, enrollment, and data and specimen collection approaches to continue their research endeavors in a way that maximized the safety of both the research participants and the research teams.

The community transformation map: A maturity tool for planning change in community health improvement for equity and well-being.

Transforming communities to be healthier and more equitable prosents a systemic challenge best addressed by those with native knowledge of the system. Community coalitions are a promising structure for tackling local health inequities, if they approach the change process with multiple local stakeholders and with systemic change in mind. Maturity models offer a framework for system assessment by defining sequential stages toward ideal development.

Antibody against integrin lymphocyte function-associated antigen 1 inhibits HIV type 1 infection in primary cells through caspase-8-mediated apoptosis.

HIV-1 infection induces formation of a virological synapse wherein CD4, chemokine receptors, and cell-adhesion molecules such as lymphocyte function-associated antigen 1 (LFA-1) form localized domains on the cell surface. Studies show that LFA-1 on the surface of HIV-1 particles retains its adhesion function and enhances virus attachment to susceptible cells by binding its counterreceptor intercellular adhesion molecule 1 (ICAM-1). This virus-cell interaction augments virus infectivity by facilitating binding and entry events.

Loss of Niemann Pick type C proteins 1 and 2 greatly enhances HIV infectivity and is associated with accumulation of HIV Gag and cholesterol in late endosomes/lysosomes.

Background: Cholesterol pathways play an important role at multiple stages during the HIV-1 infection cycle. Here, we investigated the role of cholesterol trafficking in HIV-1 replication utilizing Niemann-Pick Type C disease (NPCD) cells as a model system.

Results: We used a unique NPC2-deficient cell line (NPCD55) that exhibited Gag accumulation as well as decreased NPC1 expression after HIV infection.

Deficiency of niemann-pick type C-1 protein impairs release of human immunodeficiency virus type 1 and results in Gag accumulation in late endosomal/lysosomal compartments.

Human immunodeficiency virus type 1 (HIV-1) relies on cholesterol-laden lipid raft membrane microdomains for entry into and egress out of susceptible cells. In the present study, we examine the need for intracellular cholesterol trafficking pathways with respect to HIV-1 biogenesis using Niemann-Pick type C-1 (NPC1)-deficient (NPCD) cells, wherein these pathways are severely compromised, causing massive accumulation of cholesterol in late endosomal/lysosomal (LE/L) compartments. We have found that induction of an NPC disease-like phenotype through treatment of various cell types with the commonly used hydrophobic amine drug U18666A resulted in profound suppression of HIV-1 release.