Increased CXCR3+ T Cells Impairs Recruitment of T-Helper Type 17 Cells via Interferon γ and Interleukin 18 in the Small Intestine Mucosa During Treated HIV-1 Infection.

The restoration of CD4+ T cells, especially T-helper type 17 (Th17) cells, remains incomplete in the gut mucosa of most human immunodeficiency virus type 1 (HIV-1)-infected individuals despite sustained antiretroviral therapy (ART). Herein, we report an increase in the absolute number of CXCR3+ T cells in the duodenal mucosa during ART. The frequencies of Th1 and CXCR3+ CD8+ T cells were increased and negatively correlated with CCL20 and CCL25 expression in the mucosa. In ex vivo analyses, we showed that interferon γ, the main cytokine produced by Th1 and effector CD8+ T cells, downregulates the expression of CCL20 and CCL25 by small intestine enterocytes, while it increases the expression of CXCL9/10/11, the ligands of CXCR3. Interleukin 18, a pro-Th1 cytokine produced by enterocytes, also contributes to the downregulation of CCL20 expression and increases interferon γ production by Th1 cells. This could perpetuate an amplification loop for CXCR3-driven Th1 and effector CD8+ T cells recruitment to the gut, while impairing Th17 cells homing through the CCR6-CCL20 axis in treated HIV-1-infected individuals.

Spread of infectious chronic bee paralysis virus by honeybee (Apis mellifera L.) feces.

Knowledge of the spreading mechanism of honeybee pathogens within the hive is crucial to our understanding of bee disease dynamics. The aim of this study was to assess the presence of infectious chronic bee paralysis virus (CBPV) in bee excreta and evaluate its possible role as an indirect route of infection. Samples of paralyzed bees were (i) produced by experimental inoculation with purified virus and (ii) collected from hives exhibiting chronic paralysis. CBPV in bee heads or feces (crude or absorbed onto paper) was detected by reverse transcription-PCR. CBPV infectivity was assessed by intrathoracic inoculation of bees with virus extracted from feces and by placement of naive bees in cages previously occupied by contaminated individuals. CBPV RNA was systematically detected in the feces of naturally and experimentally infected bees and on the paper sheets that had been used to cover the floors of units containing bees artificially infected with CBPV or the floor of one naturally infected colony. Both intrathoracic inoculation of bees with virus extracted from feces and placement of bees in contaminated cages provoked overt disease in naive bees, thereby proving that the excreted virus was infectious and that this indirect route of infection could lead to overt chronic paralysis. This is the first experimental confirmation that infectious CBPV particles excreted in the feces of infected bees can infect naive bees and provoke overt disease by mere confinement of naive bees in a soiled environment.