scholarly journals Early Immune Response and Cytokine Induction of PBMC‐derived Bovine Macrophages to Infection with Rift Valley Fever Virus in the Presence and Absence of Culex tarsalis Mosquito Saliva

2021 ◽  
Vol 35 (S1) ◽  
Author(s):  
Erin Schirtzinger ◽  
William Wilson ◽  
Anne Davis
Keyword(s):  
Immune Response ◽  
Rift Valley ◽  
Rift Valley Fever ◽  
Rift Valley Fever Virus ◽  
Fever Virus ◽  
Culex Tarsalis ◽  
Valley Fever ◽  
Early Immune Response ◽  
Cytokine Induction ◽  
Mosquito Saliva

scholarly journals MVA Vectored Vaccines Encoding Rift Valley Fever Virus Glycoproteins Protect Mice against Lethal Challenge in the Absence of Neutralizing Antibody Responses

Vaccines ◽  
2020 ◽  
Vol 8 (1) ◽  
pp. 82 ◽  
Author(s):  
Elena López-Gil ◽  
Sandra Moreno ◽  
Javier Ortego ◽  
Belén Borrego ◽  
Gema Lorenzo ◽  
...  
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Cellular Immunity ◽  
Rift Valley ◽  
Neutralizing Antibodies ◽  
Rift Valley Fever ◽  
Rift Valley Fever Virus ◽  
Fever Virus ◽  
Valley Fever

In vitro neutralizing antibodies have been often correlated with protection against Rift Valley fever virus (RVFV) infection. We have reported previously that a single inoculation of sucrose-purified modified vaccinia Ankara (MVA) encoding RVFV glycoproteins (rMVAGnGc) was sufficient to induce a protective immune response in mice after a lethal RVFV challenge. Protection was related to the presence of glycoprotein specific CD8+ cells, with a low-level detection of in vitro neutralizing antibodies. In this work we extended those observations aimed to explore the role of humoral responses after MVA vaccination and to study the contribution of each glycoprotein antigen to the protective efficacy. Thus, we tested the efficacy and immune responses in BALB/c mice of recombinant MVA viruses expressing either glycoprotein Gn (rMVAGn) or Gc (rMVAGc). In the absence of serum neutralizing antibodies, our data strongly suggest that protection of vaccinated mice upon the RVFV challenge can be achieved by the activation of cellular responses mainly directed against Gc epitopes. The involvement of cellular immunity was stressed by the fact that protection of mice was strain dependent. Furthermore, our data suggest that the rMVA based single dose vaccination elicits suboptimal humoral immune responses against Gn antigen since disease in mice was exacerbated upon virus challenge in the presence of rMVAGnGc or rMVAGn immune serum. Thus, Gc-specific cellular immunity could be an important component in the protection after the challenge observed in BALB/c mice, contributing to the elimination of infected cells reducing morbidity and mortality and counteracting the deleterious effect of a subneutralizing antibody immune response.

scholarly journals Wolbachia effects on Rift Valley fever virus infection in Culex tarsalis mosquitoes

2017 ◽  
Vol 11 (10) ◽  
pp. e0006050 ◽  
Author(s):  
Brittany L. Dodson ◽  
Elizabeth S. Andrews ◽  
Michael J. Turell ◽  
Jason L. Rasgon
Keyword(s):  
Virus Infection ◽  
Rift Valley ◽  
Rift Valley Fever ◽  
Rift Valley Fever Virus ◽  
Fever Virus ◽  
Culex Tarsalis ◽  
Valley Fever

Microencapsulated plasmids expressing Gn and Gc glycoproteins of Rift Valley Fever virus enhance humoral immune response in mice

2020 ◽  
Vol 42 (4) ◽  
pp. 529-536
Author(s):  
Oxana Selina ◽  
Ilnaz Imatdinov ◽  
Vera Balysheva ◽  
Roman Akasov ◽  
Alexander Kryukov ◽  
...  
Keyword(s):  
Immune Response ◽  
Humoral Immune Response ◽  
Rift Valley ◽  
Rift Valley Fever ◽  
Rift Valley Fever Virus ◽  
Fever Virus ◽  
Valley Fever ◽  
Humoral Immune

scholarly journals Innate Immune Response to Rift Valley Fever Virus in Goats

2012 ◽  
Vol 6 (4) ◽  
pp. e1623 ◽  
Author(s):  
Charles K. Nfon ◽  
Peter Marszal ◽  
Shunzhen Zhang ◽  
Hana M. Weingartl
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Rift Valley ◽  
Rift Valley Fever ◽  
Rift Valley Fever Virus ◽  
Innate Immune ◽  
Fever Virus ◽  
Valley Fever

scholarly journals Wolbachia effects on Rift Valley fever virus infection in Culex tarsalis mosquitoes

2017 ◽  
Author(s):  
Brittany L. Dodson ◽  
Elizabeth S. Andrews ◽  
Michael J. Turell ◽  
Jason L. Rasgon
Keyword(s):  
West Nile Virus ◽  
Virus Infection ◽  
Rift Valley ◽  
Rift Valley Fever ◽  
Rift Valley Fever Virus ◽  
Mosquito Species ◽  
West Nile Virus Infection ◽  
Fever Virus ◽  
Culex Tarsalis ◽  
Valley Fever

AbstractInnovative tools are needed to alleviate the burden of mosquito-borne diseases, and strategies that target the pathogen instead of the mosquito are being considered. A possible tactic is the use of Wolbachia, a maternally inherited, endosymbiotic bacterium that can suppress diverse pathogens when introduced to naive mosquito species. We investigated effects of somatic Wolbachia (strain wAlbB) infection on Rift Valley fever virus (RVFV) in Culex tarsalis mosquitoes. When compared to Wolbachia-uninfected mosquitoes, there was no significant effect of Wolbachia infection on RVFV infection, dissemination, or transmission frequencies, nor on viral body or saliva titers. Within Wolbachia-infected mosquitoes, there was a modest negative correlation between RVFV body titers and Wolbachia density, suggesting that Wolbachia may suppress RVFV in a density-dependent manner in this mosquito species. These results are contrary to previous work in the same mosquito species, showing Wolbachia-induced enhancement of West Nile virus infection rates. Taken together, these results highlight the importance of exploring the breadth of phenotypes induced by Wolbachia.Author SummaryAn integrated vector management program utilizes several practices, including pesticide application and source reduction, to reduce mosquito populations. However, mosquitoes are developing resistance to some of these methods and new control approaches are needed. A novel technique involves the bacterium Wolbachia that lives naturally in many insects. Wolbachia can be transferred to uninfected mosquitoes and can block pathogen transmission to humans. Additionally, Wolbachia is maternally inherited, allowing it to spread quickly through uninfected field populations of mosquitoes. We studied the impacts of Wolbachia on Rift Valley fever virus (RVFV) in the naturally uninfected mosquito, Culex tarsalis. Wolbachia had no effects on the ability of Culex tarsalis to become infected with or transmit RVFV. High densities of Wolbachia were associated with no virus infection or low levels of virus, suggesting that Wolbachia might suppress RVFV at high densities. These results contrast with our previous study that showed Wolbachia enhances West Nile virus infection in Culex tarsalis. Together, these studies highlight the importance of studying Wolbachia effects on a variety of pathogens so that control methods are not impeded.

scholarly journals MAVS mediates a protective immune response in the brain to Rift Valley fever virus

2021 ◽  
Author(s):  
Dina R. Weilhammer ◽  
Nicholas R. Hum ◽  
Feliza A. Bourguet ◽  
Aimy Sebastian ◽  
Doris Lam ◽  
...  
Keyword(s):  
Immune Response ◽  
Rift Valley ◽  
Rift Valley Fever ◽  
Molecular Mechanisms ◽  
Rift Valley Fever Virus ◽  
Fever Virus ◽  
Type I ◽  
Activation Markers ◽  
Valley Fever ◽  
The Brain

Rift Valley fever virus (RVFV) is a highly pathogenic mosquito-borne virus capable of causing hepatitis, encephalitis, blindness, hemorrhagic syndrome, and death in humans and livestock. Upon aerosol infection with RVFV, the brain is a major site of viral replication and tissue damage, yet pathogenesis in this organ has been understudied. Here, we investigated the immune response in the brain of RVFV infected mice. In response to infection, microglia initiate robust transcriptional upregulation of antiviral immune genes, as well as increased levels of activation markers and cytokine secretion that is dependent on mitochondrial antiviral-signaling protein (MAVS) and independent of toll-like receptors 3 and 7. In vivo, Mavs-/- mice displayed enhanced susceptibility to RVFV as determined by increased brain viral burden and higher mortality. Single-cell RNA sequence analysis identified microglia-specific defects in type I interferon and interferon responsive gene expression in Mavs-/- mice, as well as dysregulated lymphocyte infiltration. The results of this study provide a crucial step towards understanding the precise molecular mechanisms by which RVFV infection is controlled in the brain and will help inform the development of vaccines and antiviral therapies that are effective in preventing encephalitis.

scholarly journals Laboratory demonstration of the vertical transmission of Rift Valley fever virus by Culex tarsalis mosquitoes

2021 ◽  
Vol 15 (3) ◽  
pp. e0009273
Author(s):  
Nicholas A. Bergren ◽  
Erin M. Borland ◽  
Daniel A. Hartman ◽  
Rebekah C. Kading
Keyword(s):  
Vertical Transmission ◽  
Rift Valley ◽  
Rift Valley Fever ◽  
Rift Valley Fever Virus ◽  
Preliminary Evidence ◽  
Fever Virus ◽  
Oral Exposure ◽  
Culex Tarsalis ◽  
Valley Fever ◽  
Field Evidence

Rift Valley fever virus (RVFV) is a mosquito-transmitted virus with proven ability to emerge into naïve geographic areas. Limited field evidence suggests that RVFV is transmitted vertically from parent mosquito to offspring, but until now this mechanism has not been confirmed in the laboratory. Furthermore, this transmission mechanism has allowed for the prediction of RVFV epizootics based on rainfall patterns collected from satellite information. However, in spite of the relevance to the initiation of epizootic events, laboratory confirmation of vertical transmission has remained an elusive research aim for thirty-five years. Herein we present preliminary evidence of the vertical transmission of RVFV by Culex tarsalis mosquitoes after oral exposure to RVFV. Progeny from three successive gonotrophic cycles were reared to adults, with infectious RVFV confirmed in each developmental stage. Virus was detected in ovarian tissues of parental mosquitoes 7 days after imbibing an infectious bloodmeal. Infection was confirmed in progeny as early as the first gonotrophic cycle, with infection rates ranging from 2.0–10.0%. Virus titers among progeny were low, which may indicate a host mechanism suppressing replication.

scholarly journals Aedes Mosquito Saliva Modulates Rift Valley Fever Virus Pathogenicity

2013 ◽  
Vol 7 (6) ◽  
pp. e2237 ◽  
Author(s):  
Alain Le Coupanec ◽  
Divya Babin ◽  
Laurence Fiette ◽  
Grégory Jouvion ◽  
Patrick Ave ◽  
...  
Keyword(s):  
Rift Valley ◽  
Rift Valley Fever ◽  
Rift Valley Fever Virus ◽  
Fever Virus ◽  
Aedes Mosquito ◽  
Valley Fever ◽  
Mosquito Saliva

scholarly journals Exosomes originating from infection with the cytoplasmic single-stranded RNA virus Rift Valley fever virus (RVFV) protect recipient cells by inducing RIG-I mediated IFN-B response that leads to activation of autophagy

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Farhang Alem ◽  
Adeyemi A. Olanrewaju ◽  
Samson Omole ◽  
Heather E. Hobbs ◽  
Noor Ahsan ◽  
...  
Keyword(s):  
Immune Response ◽  
Immune Cells ◽  
Rift Valley ◽  
Rift Valley Fever ◽  
Rna Viruses ◽  
Rift Valley Fever Virus ◽  
Mechanistic Model ◽  
Fever Virus ◽  
Viral Rna ◽  
Valley Fever

Abstract Background Although multiple studies have demonstrated a role for exosomes during virus infections, our understanding of the mechanisms by which exosome exchange regulates immune response during viral infections and affects viral pathogenesis is still in its infancy. In particular, very little is known for cytoplasmic single-stranded RNA viruses such as SARS-CoV-2 and Rift Valley fever virus (RVFV). We have used RVFV infection as a model for cytoplasmic single-stranded RNA viruses to address this gap in knowledge. RVFV is a highly pathogenic agent that causes RVF, a zoonotic disease for which no effective therapeutic or approved human vaccine exist. Results We show here that exosomes released from cells infected with RVFV (designated as EXi-RVFV) serve a protective role for the host and provide a mechanistic model for these effects. Our results show that treatment of both naïve immune cells (U937 monocytes) and naïve non-immune cells (HSAECs) with EXi-RVFV induces a strong RIG-I dependent activation of IFN-B. We also demonstrate that this strong anti-viral response leads to activation of autophagy in treated cells and correlates with resistance to subsequent viral infection. Since we have shown that viral RNA genome is associated with EXi-RVFV, RIG-I activation might be mediated by the presence of packaged viral RNA sequences. Conclusions Using RVFV infection as a model for cytoplasmic single-stranded RNA viruses, our results show a novel mechanism of host protection by exosomes released from infected cells (EXi) whereby the EXi activate RIG-I to induce IFN-dependent activation of autophagy in naïve recipient cells including monocytes. Because monocytes serve as reservoirs for RVFV replication, this EXi-RVFV-induced activation of autophagy in monocytes may work to slow down or halt viral dissemination in the infected organism. These findings offer novel mechanistic insights that may aid in future development of effective vaccines or therapeutics, and that may be applicable for a better molecular understanding of how exosome release regulates innate immune response to other cytoplasmic single-stranded RNA viruses.

Sign in / Sign up

Export Citation Format

Share Document