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Title: Genomics of novel influenza A virus (H18N12) in bats, Caribe Colombia
Influenza viruses are highly capable of mutating and adapting in mammalian hosts. While these viruses have been extensively studied in birds, research on their presence in bats has been limited. However, influenza viruses circulating in bats have shown notable molecular divergence. The present study aimed to characterize the phylogenetic, evolutionary, and antigenic relationships of an influenza A virus detected in the fishing bat Noctilio albiventris. As part of a pathogen surveillance study of public health interest, 159 rectal samples were collected from bats in the Colombian Caribbean. The samples were sequenced using RNA-Seq. A genome (eight viral contigs) associated with the Orthomyxoviridae family was identified in a pool. Most segments showed approximately 90% similarity with H18N11, except for the neuraminidase. Analysis of the N protein shows that occupies a basal position relative to the N11 subtype, with its divergence date estimated to be approximately 50 years earlier than the earliest reported N11 sequence. 3D modeling identified three mutations (K363R, T242K, and I139V), which may enhance interaction with the HLA-DR of bats. The analyses and antigenic divergence observed in the N protein of N. albiventris suggests the existence of a new subtype (H18N12) with unknown pathogenicity, which requires further investigation. more »« less
Crowley, Daniel E; Falvo, Caylee A; Benson, Evelyn; Hedges, Jodi; Jutila, Mark; Ezzatpour, Shahrzad; Aguilar, Hector C; Ruiz-Aravena, Manuel; Ma, Wenjun; Schountz, Tony; et al
(, PLOS Biology)
Streicker, Daniel G
(Ed.)
Bats are reservoirs of many zoonotic viruses that are fatal in humans but do not cause disease in bats. Moreover, bats generate low neutralizing antibody titers in response to experimental viral infection, although more robust antibody responses have been observed in wild-caught bats during times of food stress. Here, we compared the antibody titers and B cell receptor (BCR) diversity of Jamaican fruit bats (Artibeus jamaicensis; JFBs) and BALB/c mice generated in response to T-dependent and T-independent antigens. We then manipulated the diet of JFBs and challenged them with H18N11 influenza A-like virus or a replication incompetent Nipah virus VSV (Nipah-riVSV). Under standard housing conditions, JFBs generated a lower avidity antibody response and possessed more BCR mRNA diversity compared to BALB/c mice. However, withholding protein from JFBs improved serum neutralization in response to Nipah-riVSV and improved serum antibody titers specific to H18 but reduced BCR mRNA diversity.
Kent, Cody M.; Bevins, Sarah N.; Mullinax, Jennifer M.; Sullivan, Jeffery D.; Prosser, Diann J.
(, Ecological Applications)
Abstract Influenza A viruses in wild birds pose threats to the poultry industry, wild birds, and human health under certain conditions. Of particular importance are wild waterfowl, which are the primary reservoir of low‐pathogenicity influenza viruses that ultimately cause high‐pathogenicity outbreaks in poultry farms. Despite much work on the drivers of influenza A virus prevalence, the underlying viral subtype dynamics are still mostly unexplored. Nevertheless, understanding these dynamics, particularly for the agriculturally significant H5 and H7 subtypes, is important for mitigating the risk of outbreaks in domestic poultry farms. Here, using an expansive surveillance database, we take a large‐scale look at the spatial, temporal, and taxonomic drivers in the prevalence of these two subtypes among influenza A‐positive wild waterfowl. We document spatiotemporal trends that are consistent with past work, particularly an uptick in H5 viruses in late autumn and H7 viruses in spring. Interestingly, despite large species differences in temporal trends in overall influenza A virus prevalence, we document only modest differences in the relative abundance of these two subtypes and little, if any, temporal differences among species. As such, it appears that differences in species' phenology, physiology, and behaviors that influence overall susceptibility to influenza A viruses play a much lesser role in relative susceptibility to different subtypes. Instead, species are likely to freely pass viruses among each other regardless of subtype. Importantly, despite the similarities among species documented here, individual species still may play important roles in moving viruses across large geographic areas or sustaining local outbreaks through their different migratory behaviors.
The greatest challenge to preventing the next influenza pandemic is the extensive diversity within the influenza virus family ( 1 ). At present, 20 lineages of influenza A and B viruses have been identified, each containing numerous strains ( 2 , 3 ). Current influenza vaccines, composed of four influenza viral antigens, provide little protection beyond the viral strains targeted by the vaccines. Universal influenza vaccines that can protect against all 20 lineages could help to prevent the next pandemic ( 4 ). Designing and manufacturing a vaccine that can provide such broad protection has been challenging, but the demonstration of the feasibility of mRNA–lipid nanoparticle COVID-19 vaccines offers a possible strategy ( 5 ). On page 899 of this issue, Arevalo et al. ( 6 ) report an influenza vaccine, using mRNA–lipid nanoparticle technology incorporating representatives of all 20 influenza virus lineages, that protected mice and ferrets from diverse influenza viruses. This provides a pathway to a universal influenza vaccine.
Phillips, Angela M; Gonzalez, Luna O; Nekongo, Emmanuel E; Ponomarenko, Anna I; McHugh, Sean M; Butty, Vincent L; Levine, Stuart S; Lin, Yu-Shan; Mirny, Leonid A; Shoulders, Matthew D
(, eLife)
Influenza viruses, commonly called flu, can evade our immune system and develop resistance to treatments by changing frequently. Specifically, mutations in their genome cause influenza proteins to change in ways that can help the virus evade our defences. However, these mutations come at a cost and can prevent the viral proteins from forming functional and stable three-dimensional shapes – a process known as protein folding – thereby hampering the virus’ ability to replicate. In human cells, proteins called chaperones can help our other proteins fold properly. Influenza viruses do not have their own chaperones and, instead, hijack those of their host. Host chaperones are therefore crucial to the virus’ ability to replicate. However, until now, it was not known if host chaperones can influence how these viruses evolve. Here, Phillips et al. used mammalian cells to study how host chaperones affect an evolving influenza population. First, cells were engineered to either have normal chaperone levels, elevated chaperone levels, or inactive chaperones. Next, the H3N2 influenza strain was grown in these different conditions for nearly 200 generations and sequenced to determine how the virus evolved in each distinctive host chaperone environment. Phillips et al. discovered that host chaperones affect the rate at which mutations accumulate in the influenza population, and also the types of mutations in the influenza genome. For instance, when a chaperone called Hsp90 was inactivated, mutations became prevalent in the viral population more slowly than in cells with normal or elevated chaperone levels. Moreover, some specific mutations fared better in cells with high chaperone levels, whilst others worked better in cells with inactivated chaperones. These results suggest that influenza evolution is affected by host chaperone levels in complex and important ways. Moreover, whether chaperones will promote or hinder the effects of any single mutation is difficult to predict ahead of time. This discovery is significant, as the chaperones available to influenza can vary in different tissues, organisms and infectious conditions, and may therefore influence the virus' ability to change and evolve in a context-specific manner. The findings are likely to extend to other viruses such as HIV and Ebola, which also hijack host chaperones for the same purpose. More work is now needed to systematically quantify these effects so that we can better predict how specific chaperones will affect the ability of viruses to adapt, especially in pathologically relevant conditions like fever or viral host-switching. In the future, such insights could help shape the design of treatments to which viruses do not evolve resistance.
Falvo, Caylee A; Crowley, Daniel E; Benson, Evelyn; Hall, Monica N; Schwarz, Benjamin; Bohrnsen, Eric; Ruiz-Aravena, Manuel; Hebner, Madison; Ma, Wenjun; Schountz, Tony; et al
(, Proceedings of the Royal Society B: Biological Sciences)
Land-use change may drive viral spillover from bats into humans, partly through dietary shifts caused by decreased availability of native foods and increased availability of cultivated foods. We experimentally manipulated diets of Jamaican fruit bats to investigate whether diet influences viral shedding. To reflect dietary changes experienced by wild bats during periods of nutritional stress, Jamaican fruit bats were fed either a standard diet or a putative suboptimal diet, which was deprived of protein (suboptimal-sugar diet) and/or supplemented with fat (suboptimal-fat diet). Upon H18N11 influenza A-virus infection, bats fed on the suboptimal-sugar diet shed the most viral RNA for the longest period, but bats fed the suboptimal-fat diet shed the least viral RNA for the shortest period. Bats on both suboptimal diets ate more food than the standard diet, suggesting nutritional changes may alter foraging behaviour. This study serves as an initial step in understanding whether and how dietary shifts may influence viral dynamics in bats, which alters the risk of spillover to humans.
@article{osti_10595278,
place = {Country unknown/Code not available},
title = {Genomics of novel influenza A virus (H18N12) in bats, Caribe Colombia},
url = {https://par.nsf.gov/biblio/10595278},
DOI = {10.1038/s41598-025-91026-8},
abstractNote = {Influenza viruses are highly capable of mutating and adapting in mammalian hosts. While these viruses have been extensively studied in birds, research on their presence in bats has been limited. However, influenza viruses circulating in bats have shown notable molecular divergence. The present study aimed to characterize the phylogenetic, evolutionary, and antigenic relationships of an influenza A virus detected in the fishing bat Noctilio albiventris. As part of a pathogen surveillance study of public health interest, 159 rectal samples were collected from bats in the Colombian Caribbean. The samples were sequenced using RNA-Seq. A genome (eight viral contigs) associated with the Orthomyxoviridae family was identified in a pool. Most segments showed approximately 90% similarity with H18N11, except for the neuraminidase. Analysis of the N protein shows that occupies a basal position relative to the N11 subtype, with its divergence date estimated to be approximately 50 years earlier than the earliest reported N11 sequence. 3D modeling identified three mutations (K363R, T242K, and I139V), which may enhance interaction with the HLA-DR of bats. The analyses and antigenic divergence observed in the N protein of N. albiventris suggests the existence of a new subtype (H18N12) with unknown pathogenicity, which requires further investigation.},
journal = {Scientific Reports},
volume = {15},
number = {1},
publisher = {Nature},
author = {Echeverri-De_la_Hoz, Daniel and Martínez-Bravo, Caty and Gastelbondo-Pastrana, Bertha and Rivero, Ricardo and López, Yesica and Bertel, Valeria and Alemán-Santos, Maira and Garay, Evelin and Hoyos, Richard and Arrieta, Germán and Ramírez, Juan David and Mattar, Salim},
}
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