Publications by authors named "Margarita V Rangel"
Neurotropic alphaviruses such as Venezuelan equine encephalitis virus (VEEV) are critical human pathogens that continually expand to naïve populations and for which there are no licensed vaccines or therapeutics. VEEV is highly infectious via the aerosol route and is a recognized weaponizable biothreat that causes neurological disease in humans. The neuropathology of VEEV has been attributed to an inflammatory immune response in the brain yet the underlying mechanisms and specific immune cell populations involved are not fully elucidated.
View Article and Find Full Text PDFCoccidioidomycosis, or Valley fever, is a lung disease caused by inhalation of fungi, prevalent in the Southwestern United States, Mexico, and parts of Central and South America. Annually, the United States reports 10,000-20,000 cases, although those numbers are expected to increase as climate change expands the fungal geographic range. While 60% of infections are asymptomatic, 40% symptomatic infections are often misdiagnosed due to similarities with bronchitis or pneumonia.
View Article and Find Full Text PDFRift Valley fever phlebovirus (RVFV) is a highly pathogenic mosquito-borne virus with bioweapon potential due to its ability to be spread by aerosol transmission. Neurological symptoms are among the worst outcomes of infection, and understanding of pathogenesis mechanisms within the brain is limited. RVFV is classified as an overlap select agent by the CDC and USDA; therefore, experiments involving fully virulent strains of virus are tightly regulated.
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- Chikungunya virus (CHIKV) is a serious health risk and understanding its disease mechanisms and replication is vital for public health efforts.
- Research identified two key mutations (E1 V156A and E1 K211T) in the CHIKV glycoprotein that enhance the virus's ability to infect and cause disease in hosts, including humans.
- These mutations alter how the virus interacts with host cells, leading to increased infectivity and symptoms like foot swelling in mouse models, highlighting the need for further studies on CHIKV variants.
Article Synopsis
- Alphaviruses and flaviviruses have similar class II fusion glycoproteins crucial for their assembly and infectivity, specifically noting conservation in the tip of domain II among both virus families.
- Research on Zika virus identified a novel envelope glycoprotein variant that, while minimally affecting infection in mosquitoes, reduced viral replication in human cells and mice and heightened sensitivity to ammonium chloride.
- The study further explored mutations in the flavivirus E β-strand c and ij loop, revealing that certain alterations can inhibit the production of infectious Zika and yellow fever viruses, suggesting that structural similarities in these glycoproteins play significant roles in viral infection and could inform antiviral strategies.
Alphaviruses are important pathogens that continue to cause outbreaks of disease in humans and animals worldwide. Diseases caused by alphavirus infections include acute symptoms of fever, rash, and nausea as well as chronic arthritis and severe-to-fatal conditions including myocarditis and encephalitis. Despite their prevalence and the significant public health threat they pose, there are currently no effective antiviral treatments or vaccines against alphaviruses.
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- Researchers created a system using immunocompromised mice to study how Zika virus (ZIKV) evolves during infection, focusing on its transmission and characteristics.
- They found that the way ZIKV is transmitted and the specific environments in different organs affect the virus's diversity and the types of defective genomes produced.
- The study also discovered ZIKV mutants that aligned with strains circulating in Asia and America, as well as unique mutations from the mouse model, enhancing our understanding of arbovirus evolution and the factors that influence it.
Understanding the fundamental mechanisms of arbovirus transmission and pathogenesis is essential to develop strategies for treatment and prevention. We previously took an in vivo evolution-based approach and identified the chikungunya virus E1 glycoprotein residue 80 to play a critical role in viral transmission and pathogenesis. In this study, we address the genetic conservation and function of position 80 and demonstrate that this residue is a key determinant in alphavirus infectivity and dissemination through modulation of viral fusion and cholesterol dependence.
View Article and Find Full Text PDFWe characterized an operon in , Rv3679-Rv3680, in which each open reading frame is annotated to encode "anion transporter ATPase" homologues. Using structure prediction modeling, we found that Rv3679 and Rv3680 more closely resemble the uided ntry of ail-anchored proteins (Get3) chaperone in eukaryotes. Get3 delivers proteins into the membranes of the endoplasmic reticulum and is essential for the normal growth and physiology of some eukaryotes.
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