Benjamin M Althouse | Search bioRxiv

bioRxiv2016

Monkey in the middle: monkeys serve as amplification hosts but not reservoir hosts of sylvatic chikungunya virus

Athropod-borne viruses (arboviruses) pose the greatest risk of spillover into humans of any class of pathogens. Such spillover may occur as a one-step jump from a reservoir host species into humans or as a two-step jump from the reservoir to a different amplification host species and thence to humans. Despite the widespread havoc wreaked by emerging arboviruses, little is known about their transmission dynamics in reservoir and amplification hosts. Here we used serosurveillance and mathematical modeling to elucidate the role of monkeys in the sylvatic, enzootic cycle of chikungunya virus (CHIKV). Over three years, 219 African green monkeys, 78 patas monkeys, and 440 Guinea baboons were captured in the region surrounding Kedougou, Senegal. The age of each animal was determined by anthropometry and dentition, and exposure to CHIKV was determined by detection of neutralizing antibodies. We estimate age-specific CHIKV seroprevalence, force of infection (FoI), and basic reproductive number (R0) in each species. Among the different species, CHIKV Fol ranged from 0.13 to 1.12 (95% CI, 0.81-2.28) and R0 ranged from 1.5 (95% CI, 1.3-1.9) to 6.6 (95% CI, 5.1-10.4). CHIKV infection of infant monkeys was detected even when the virus was not detected in a concurrent survey of primatophilic mosquitoes and when population seropositivity, and therefore immunity, was too high for monkeys themselves to support continuous CHIKV transmission. We therefore conclude that monkeys in this region serve primarily as amplification rather than reservoir hosts of CHIKV. Additional efforts are needed to identify other vertebrate hosts capable of supporting continuous circulation.

Ecology↗

bioRxiv2016

Analysis of clinical Bordetella pertussis isolates using whole genome sequences reveals novel genomic regions associated with recent outbreaks in the United States of America

BackgroundDespite high-levels of vaccination, whooping cough, primarily caused by Bordetella pertussis (BP), has persisted and resurged. It remains a major cause of infant death worldwide and is the most prevalent vaccine-preventable disease in developed countries. To date, most genomic studies have focused on a small subset of the BP genome, biasing our clinical understanding and public health awareness.\n\nMethodsWe performed a Genome-Wide Association Study (GWAS) on 76 U.S. BP whole genomes, including strains from recent outbreaks.\n\nResultsA GWAS of the 76 BP isolates revealed a sharp increase in genetic variation associated with the Minnesota 2012 outbreak and identified 52 variants unique to the Minnesota outbreak and 19 unique to the California and Washington outbreaks. None of the identified variants were shared between the outbreaks and the vast majority were previously uncharacterized. We further identified variation associated with pertactin negative strains and acellular vaccination.\n\nConclusionsWe identified novel genomic regions associated with recent BP outbreaks. Our results underscore the need for increased whole genome sequencing of BP isolates, which can reduce costly misdiagnosis and improve surveillance. The genes containing these variants warrant further investigation into their possible roles in BP pathogenicity and the ongoing resurgence in the U.S.

Genomics↗