Poster Session II
Project Type
Poster
Project Funding and Affiliations
Luis Lab- University of Montana
Faculty Mentor’s Full Name
Angela Luis
Faculty Mentor’s Department
Department of Ecosystem and Conservation Science
Additional Mentor
nelle.jenkins@umconnect.umt.edu
Abstract / Artist's Statement
Sin Nombre virus (SNV) is a New World RNA virus within the family of Hantiviridae found primarily in North America. SNV is a zoonotic pathogen, causing unapparent disease in its deer mouse (Peromyscus maniculatus) reservoir host, but inducing Hantavirus Pulmonary Syndrome, a respiratory infection of pulmonary endothelial cells, in its human hosts. The virus is transmitted primarily through aerosolized rodent excreta.
Previous studies of the SNV genome has identified the virus as a negative-sense single-stranded RNA pathogen: its segmented genome consists of RNA that is the reverse complement of the mRNA needed to make proteins. The -ssRNA genome consists of an S, M, and L segment important for reassortment and viral evolution. This capstone project analyzes the microevolution of Sin Nombre virus using PCR probe matching informed by prior genomic work conducted in the Luis Lab.
Initial screening was conducted using enzyme-linked immunosorbent assays (ELISAs) to detect Sin Nombre virus antibodies in P. maniculatus blood samples. Confirmatory PCR targeting the M segment will be performed to verify the presence of viral RNA in two seropositive samples from each P. maniculatus capture site. To assess microevolution of the viral genome, PCR will then be performed using S segment primers developed in a previous study conducted five years ago that correspond closely to the original probe locations. Consistent amplification would suggest conservation of the S-segment target region, while lack of amplification may indicate sequence divergence consistent with viral microevolution.
This study evaluates genetic conservation or divergence in a key region of the SNV genome, contributing to fields of virology and disease ecology in understanding how Sin Nombre virus evolves over time in its natural reservoir host. Because SNV is a segmented negative-sense RNA virus, small genetic changes can influence viral transmission, reassortment, and interactions with host immune systems. This work therefore adds to broader efforts in wildlife disease ecology to understand how zoonotic viruses persist and diversify.
Category
Life Sciences
Sin Nombre virus: Assessing Variation in the Viral Genome Across Peromyscus maniculatus Populations in Western Montana
UC South Ballroom
Sin Nombre virus (SNV) is a New World RNA virus within the family of Hantiviridae found primarily in North America. SNV is a zoonotic pathogen, causing unapparent disease in its deer mouse (Peromyscus maniculatus) reservoir host, but inducing Hantavirus Pulmonary Syndrome, a respiratory infection of pulmonary endothelial cells, in its human hosts. The virus is transmitted primarily through aerosolized rodent excreta.
Previous studies of the SNV genome has identified the virus as a negative-sense single-stranded RNA pathogen: its segmented genome consists of RNA that is the reverse complement of the mRNA needed to make proteins. The -ssRNA genome consists of an S, M, and L segment important for reassortment and viral evolution. This capstone project analyzes the microevolution of Sin Nombre virus using PCR probe matching informed by prior genomic work conducted in the Luis Lab.
Initial screening was conducted using enzyme-linked immunosorbent assays (ELISAs) to detect Sin Nombre virus antibodies in P. maniculatus blood samples. Confirmatory PCR targeting the M segment will be performed to verify the presence of viral RNA in two seropositive samples from each P. maniculatus capture site. To assess microevolution of the viral genome, PCR will then be performed using S segment primers developed in a previous study conducted five years ago that correspond closely to the original probe locations. Consistent amplification would suggest conservation of the S-segment target region, while lack of amplification may indicate sequence divergence consistent with viral microevolution.
This study evaluates genetic conservation or divergence in a key region of the SNV genome, contributing to fields of virology and disease ecology in understanding how Sin Nombre virus evolves over time in its natural reservoir host. Because SNV is a segmented negative-sense RNA virus, small genetic changes can influence viral transmission, reassortment, and interactions with host immune systems. This work therefore adds to broader efforts in wildlife disease ecology to understand how zoonotic viruses persist and diversify.