Shedding of Marburg Virus in Naturally Infected Egyptian Rousette Bats, South Africa, 2017.
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ABSTRACT:
SUBMITTER: Paweska JT
PROVIDER: S-EPMC7706944 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Marburg virus (MARV) causes sporadic outbreaks of severe Marburg virus disease (MVD). Most MVD outbreaks originated in East Africa and field studies in East Africa, South Africa, Zambia, and Gabon identified the Egyptian rousette bat (ERB; Rousettus aegyptiacus) as a natural reservoir. However, the largest recorded MVD outbreak with the highest case-fatality ratio happened in 2005 in Angola, where direct spillover from bats was not shown. Here, collaborative studies by the Centers for Disease Control and Prevention, Njala University, University of California, Davis USAID-PREDICT, and the University of Makeni identify MARV circulating in ERBs in Sierra Leone. PCR, antibody and virus isolation data from 1755 bats of 42 species shows active MARV infection in approximately 2.5% of ERBs. Phylogenetic analysis identifies MARVs that are similar to the Angola strain. These results provide evidence of MARV circulation in West Africa and demonstrate the value of pathogen surveillance to identify previously undetected threats.
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Project description:Although bats are natural reservoir hosts for numerous zoonotic viruses, little is known about the long-term dynamics of the host immune response following infection and how these viruses are maintained in nature. The Egyptian rousette bat (ERB) is a known reservoir host for Marburg virus (MARV). Following infection of ERBs with MARV, virus-specific IgG antibodies are induced but rapidly wane and by 3 months post-infection the bats are seronegative. To determine whether reinfection of ERBs plays a role in MARV maintenance, we challenge groups of ERBs that were "naturally" or experimentally infected with MARV 17-24 months prior. No bats in either group exhibit evidence of MARV replication or shedding and all bats develop virus-specific secondary immune responses. This study demonstrates that infection of ERBs with MARV induces long-term protective immunity against reinfection and indicates that other factors, such as host population dynamics, drive MARV maintenance in nature.
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Project description:In recent years, bats have been shown to host various novel bat-specific influenza viruses, including H17N10 and H18N11 in the Americas and the H9N2 subtype from Africa. Rousettus aegyptiacus (Egyptian Rousette bat) is recognized as a host species for diverse viral agents. This study focused on the molecular surveillance of a maternal colony in Limpopo, South Africa, between 2017-2018. A pan-influenza hemi-nested RT-PCR assay targeting the PB1 gene was established, and influenza A virus RNA was identified from one fecal sample out of 860 samples. Genome segments were recovered using segment-specific amplification combined with standard Sanger sequencing and Illumina unbiased sequencing. The identified influenza A virus was closely related to the H9N2 bat-influenza virus, confirming the circulation of this subtype among Egyptian fruit bat populations in Southern Africa. This bat H9N2 subtype contained amino acid residues associated with transmission and virulence in either mammalian or avian hosts, though it will likely require additional adaptations before spillover.
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Project description:The Egyptian rousette bat (ERB) is the only known Marburg virus (MARV) reservoir host. ERBs develop a productive MARV infection with low viremia and shedding but no overt disease, suggesting this virus is efficiently controlled by ERB antiviral responses. This dynamic would contrast with humans, where MARV-mediated interferon (IFN) antagonism early in infection is thought to contribute to the severe, often fatal disease. The newly-annotated ERB genome and transcriptome have now enabled us to use a custom-designed NanoString nCounter ERB CodeSet in conjunction with RNA-seq to investigate responses in a MARV-infected ERB cell line. Both transcriptomic platforms correlated well and showed that MARV inhibited the antiviral program in ERB cells, while an IFN antagonism-impaired MARV was less efficient at suppressing the response gene induction, phenotypes previously reported for primate cells. Interestingly, and despite the expansion of IFN loci in the ERB genome, neither MARV showed specific induction of almost any IFN gene. However, we detected an upregulation of putative, unannotated ERB antiviral paralogs, as well as an elevated basal expression in uninfected ERB cells of key antiviral genes.
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