scholarly journals Cool temperatures limit Zika virus genome replication

2021 ◽  
Author(s):  
Blanka Tesla ◽  
Jenna S Powers ◽  
Yvonne Barnes ◽  
Shamil Lakhani ◽  
Marissa D Acciani ◽  
...  
Keyword(s):  
Virus Replication ◽  
Zika Virus ◽  
Disease Transmission ◽  
Virus Genome ◽  
Replication Cycle ◽  
Genome Replication ◽  
Cool Temperature ◽  
Transmission Potential ◽  
Mosquito Cells ◽  
Virus Replication Cycle

Zika virus is a mosquito-borne flavivirus known to cause severe birth defects and neuroimmunological disorders. We have previously demonstrated that mosquito transmission of Zika virus decreases with temperature. While transmission was optimized at 29°C, it was limited at cool temperatures (< 22°C) due to poor virus establishment in the mosquitoes. Temperature is one of the strongest drivers of vector-borne disease transmission due to its profound effect on ectothermic mosquito vectors, viruses, and their interaction. Although there is substantial evidence of temperature effects on arbovirus replication and dissemination inside mosquitoes, little is known about whether temperature affects virus replication directly or indirectly through mosquito physiology. In order to determine the mechanisms behind temperature-induced changes in Zika virus transmission potential, we investigated different steps of the virus replication cycle in mosquito cells (C6/36) at optimal (28°C) and cool (20°C) temperatures. We found that cool temperature did not alter Zika virus entry or translation but reduced the amount of double-stranded RNA replication intermediates. If replication complexes were first formed at 28°C and the cells were subsequently shifted to 20°C, the late steps in the virus replication cycle were efficiently completed. These data suggest that cool temperature decreases the efficiency of Zika virus genome replication in mosquito cells. This phenotype was observed in the Asian-lineage of Zika virus, while the African-lineage Zika virus was less restrictive at 20°C.

scholarly journals Variable Inhibition of Zika Virus Replication by Different Wolbachia Strains in Mosquito Cell Cultures

2017 ◽  
Vol 91 (14) ◽  
Author(s):  
Michaela J. Schultz ◽  
Sharon Isern ◽  
Scott F. Michael ◽  
Ronald B. Corley ◽  
John H. Connor ◽  
...  
Keyword(s):  
Virus Replication ◽  
Zika Virus ◽  
Western Hemisphere ◽  
Mosquito Cell ◽  
Mosquito Vector ◽  
Viral Inhibition ◽  
Virus Growth ◽  
Content Type ◽  
Bacterial Endosymbiont ◽  
Mosquito Cells

ABSTRACT Mosquito-borne arboviruses are a major source of human disease. One strategy to reduce arbovirus disease is to reduce the mosquito's ability to transmit virus. Mosquito infection with the bacterial endosymbiont Wolbachia pipientis wMel is a novel strategy to reduce Aedes mosquito competency for flavivirus infection. However, experiments investigating cyclic environmental temperatures have shown a reduction in maternal transmission of wMel, potentially weakening the integration of this strain into a mosquito population relative to that of other Wolbachia strains. Consequently, it is important to investigate additional Wolbachia strains. All Zika virus (ZIKV) suppression studies are limited to the wMel Wolbachia strain. Here we show ZIKV inhibition by two different Wolbachia strains: wAlbB (isolated from Aedes albopictus mosquitoes) and wStri (isolated from the planthopper Laodelphax striatellus) in mosquito cells. Wolbachia strain wStri inhibited ZIKV most effectively. Single-cycle infection experiments showed that ZIKV RNA replication and nonstructural protein 5 translation were reduced below the limits of detection in wStri-containing cells, demonstrating early inhibition of virus replication. ZIKV replication was rescued when Wolbachia was inhibited with a bacteriostatic antibiotic. We observed a partial rescue of ZIKV growth when Wolbachia-infected cells were supplemented with cholesterol-lipid concentrate, suggesting competition for nutrients as one of the possible mechanisms of Wolbachia inhibition of ZIKV. Our data show that wAlbB and wStri infection causes inhibition of ZIKV, making them attractive candidates for further in vitro mechanistic and in vivo studies and future vector-centered approaches to limit ZIKV infection and spread. IMPORTANCE Zika virus (ZIKV) has swiftly spread throughout most of the Western Hemisphere. This is due in large part to its replication in and spread by a mosquito vector host. There is an urgent need for approaches that limit ZIKV replication in mosquitoes. One exciting approach for this is to use a bacterial endosymbiont called Wolbachia that can populate mosquito cells and inhibit ZIKV replication. Here we show that two different strains of Wolbachia, wAlbB and wStri, are effective at repressing ZIKV in mosquito cell lines. Repression of virus growth is through the inhibition of an early stage of infection and requires actively replicating Wolbachia. Our findings further the understanding of Wolbachia viral inhibition and provide novel tools that can be used in an effort to limit ZIKV replication in the mosquito vector, thereby interrupting the transmission and spread of the virus.

scholarly journals Hepatitis C virus replication cycle

2010 ◽  
Vol 53 (3) ◽  
pp. 583-585 ◽  
Author(s):  
Ralf Bartenschlager ◽  
Francois-Loic Cosset ◽  
Volker Lohmann
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Virus Replication ◽  
Replication Cycle ◽  
Virus Replication Cycle

Scavenger receptor class B member 1 ( SCARB1 ) variants modulate hepatitis C virus replication cycle and viral load

2017 ◽  
Vol 67 (2) ◽  
pp. 237-245 ◽  
Author(s):  
Sandra Westhaus ◽  
Maximilian Deest ◽  
Anna T.X. Nguyen ◽  
Frauke Stanke ◽  
Dirk Heckl ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Viral Load ◽  
Hepatitis C ◽  
Virus Replication ◽  
Scavenger Receptor ◽  
Replication Cycle ◽  
Scavenger Receptor Class ◽  
Class B ◽  
Virus Replication Cycle

scholarly journals A comprehensive map of the influenza A virus replication cycle

2013 ◽  
Vol 7 (1) ◽  
pp. 97 ◽  
Author(s):  
Yukiko Matsuoka ◽  
Hiromi Matsumae ◽  
Manami Katoh ◽  
Amie J Eisfeld ◽  
Gabriele Neumann ◽  
...  
Keyword(s):  
Influenza A Virus ◽  
Virus Replication ◽  
Influenza A ◽  
Replication Cycle ◽  
Virus Replication Cycle

scholarly journals Completion of Hepatitis C Virus Replication Cycle in Heterokaryons Excludes Dominant Restrictions in Human Non-liver and Mouse Liver Cell Lines

2011 ◽  
Vol 7 (4) ◽  
pp. e1002029 ◽  
Author(s):  
Anne Frentzen ◽  
Kathrin Hüging ◽  
Julia Bitzegeio ◽  
Martina Friesland ◽  
Sibylle Haid ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Cell Lines ◽  
Virus Replication ◽  
Liver Cell ◽  
Mouse Liver ◽  
Replication Cycle ◽  
Mouse Liver Cell ◽  
Virus Replication Cycle

In-depth characterization of the chikungunya virus replication cycle

2021 ◽  
Author(s):  
Erik V. S. Reis ◽  
Beatriz M. Damas ◽  
Diogo C. Mendonça ◽  
Jônatas S. Abrahão ◽  
Cláudio A. Bonjardim
Keyword(s):  
Virus Replication ◽  
Chikungunya Virus ◽  
Replication Cycle ◽  
New Drugs ◽  
Biological Assays ◽  
Host Interactions ◽  
Virion Release ◽  
Long Time ◽  
Membrane Protrusions ◽  
Virus Replication Cycle

The chikungunya virus has spread globally with a remarkably high attack rate. Infection causes arthralgic sequelae that can last for years. Nevertheless, there are no specific drugs or vaccines to contain the virus. Understanding the biology of the virus, such as its replication cycle, is a powerful tool to identify new drugs and comprehend virus-host interactions. Even though the chikungunya virus has been known for a long time (first described in 1952), many aspects of the replication cycle remain unclear. Furthermore, part of the cycle is based on observations of other alphaviruses. In this study, we used electron and scanning microscopy, as well as biological assays, to analyze and investigate the stages of the chikungunya virus replication cycle. Based on our data, we found other infection cellular activities than those usually described for the chikungunya virus replication cycle, i.e. we show particles enveloping intracellularly without budding in a membrane-delimited morphogenesis area; and we also observed virion release by membrane protrusions. Our work provides novel details regarding the biology of chikungunya virus and fills gaps in our knowledge of its replication cycle. These findings may contribute to a better understanding of virus-host interactions and support the development of antivirals. IMPORTANCE The understanding of virus biology is essential to containing virus dissemination, and exploring the virus replication cycle is a powerful tool to do this. There are many points in the biology of the chikungunya virus that need to be clarified, especially regarding its replication cycle. Our incomplete understanding of chikungunya virus infection stages is based on studies with other alphaviruses. We systematized the chikungunya virus replication cycle using microscopic imaging in the order of infection stages: entry, replication, protein synthesis, assembly/morphogenesis, and release. The imaging evidence shows novel points in the replication cycle of enveloping without budding, as well as particle release by cell membrane protrusion.

scholarly journals Role of the CM2 Protein in the Influenza C Virus Replication Cycle

2010 ◽  
Vol 85 (3) ◽  
pp. 1322-1329 ◽  
Author(s):  
T. Furukawa ◽  
Y. Muraki ◽  
T. Noda ◽  
E. Takashita ◽  
R. Sho ◽  
...  
Keyword(s):  
Virus Replication ◽  
Replication Cycle ◽  
Influenza C Virus ◽  
Virus Replication Cycle
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