Gender Parity Trends for Invited Speakers at Four Prominent Virology Conference Series

ABSTRACT Scientific conferences are most beneficial to participants when they showcase significant new experimental developments, accurately summarize the current state of the field, and provide strong opportunities for collaborative networking. A top-notch slate of invited speakers, assembled by conference organizers or committees, is key to achieving these goals. The perceived underrepresentation of female speakers at prominent scientific meetings is currently a popular topic for discussion, but one that often lacks supportive data. We compiled the full rosters of invited speakers over the last 35 years for four prominent international virology conferences, the American Society for Virology Annual Meeting (ASV), the International Herpesvirus Workshop (IHW), the Positive-Strand RNA Virus Symposium (PSR), and the Gordon Research Conference on Viruses & Cells (GRC). The rosters were cross-indexed by unique names, gender, year, and repeat invitations. When plotted as gender-dependent trends over time, all four conferences showed a clear proclivity for male-dominated invited speaker lists. Encouragingly, shifts toward parity are emerging within all units, but at different rates. Not surprisingly, both selection of a larger percentage of first-time participants and the presence of a woman on the speaker selection committee correlated with improved parity. Session chair information was also collected for the IHW and GRC. These visible positions also displayed a strong male dominance over time that is eroding slowly. We offer our personal interpretation of these data to aid future organizers achieve improved equity among the limited number of available positions for session moderators and invited speakers. IMPORTANCE Politicians and media members have a tendency to cite anecdotes as conclusions without any supporting data. This happens so frequently now, that a name for it has emerged: fake news. Good science proceeds otherwise. The underrepresentation of women as invited speakers at international scientific conferences exemplifies a present-day discussion topic usually occurring without facts to support or refute the arguments. We now provide records profiling four prominent virology conferences over the years 1982 to 2017 with the intention that the trends and accompanying analyses of the gender parity of invited speakers may allow the ongoing discussions to be informed.

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RNA-Protein Interaction Analysis of SARS-CoV-2 5′ and 3′ Untranslated Regions Reveals a Role of Lysosome-Associated Membrane Protein-2a during Viral Infection

mSystems ◽

10.1128/msystems.00643-21 ◽

2021 ◽

Author(s):

Rohit Verma ◽

Sandhini Saha ◽

Shiv Kumar ◽

Shailendra Mani ◽

Tushar Kanti Maiti ◽

...

Keyword(s):

Interaction Analysis ◽

Rna Virus ◽

Untranslated Regions ◽

Host Proteins ◽

Positive Strand ◽

Replication Complex ◽

Positive Strand Rna Virus ◽

Positive Strand Rna ◽

Viral Genomic Rna

Replication of a positive-strand RNA virus involves an RNA-protein complex consisting of viral genomic RNA, host RNA(s), virus-encoded proteins, and host proteins. Dissecting out individual components of the replication complex will help decode the mechanism of viral replication. 5′ and 3′ UTRs in positive-strand RNA viruses play essential regulatory roles in virus replication.

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SARS-CoV-2 Isolation and Propagation from Turkish COVID-19 patients

10.1101/2020.04.23.056309 ◽

2020 ◽

Cited By ~ 2

Author(s):

Cihan Tastan ◽

Bulut Yurtsever ◽

Gozde Sir ◽

Derya Dilek Kancagi ◽

Sevda Demir ◽

...

Keyword(s):

Rna Virus ◽

The Novel ◽

Isolation And Characterization ◽

Characterization Studies ◽

Positive Strand Rna Virus ◽

The Republic ◽

Novel Coronavirus ◽

Positive Strand Rna ◽

Vaccine Testing ◽

Republic Of Turkey

AbstractThe novel coronavirus pneumonia, which was named later as Coronavirus Disease 2019 (COVID-19), is caused by the Severe Acute Respiratory Syndrome Coronavirus 2, namely SARS-CoV-2. It is a positive-strand RNA virus that is the seventh coronavirus known to infect humans. The COVID-19 outbreak presents enormous challenges for global health behind the pandemic outbreak. The first diagnosed patient in Turkey has been reported by the Republic of Turkey Ministry of Health on March 11, 2020. Today, over ninety thousand cases in Turkey, and two million cases around the world have been declared. Due to the urgent need for vaccine and anti-viral drug, isolation of the virus is crucial. Here, we report one of the first isolation and characterization studies of SARS-CoV-2 from nasopharyngeal and oropharyngeal specimens of diagnosed patients in Turkey. This study provides an isolation and replication methodology, and cell culture tropism of the virus that will be available to the research communities.Article SummaryScientists have isolated virus from Turkish COVID-19 patients. The isolation, propagation, and plaque and immune response assays of the virus described here will serve in following drug discovery and vaccine testing.

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Mechanisms and consequences of positive-strand RNA virus recombination

Journal of General Virology ◽

10.1099/jgv.0.001142 ◽

2018 ◽

Vol 99 (10) ◽

pp. 1345-1356 ◽

Cited By ~ 17

Author(s):

Kirsten Bentley ◽

David J. Evans

Keyword(s):

Rna Virus ◽

Positive Strand ◽

Virus Recombination ◽

Positive Strand Rna Virus ◽

Positive Strand Rna

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Regulation of positive-strand RNA virus replication: The emerging role of phosphorylation

Virus Research ◽

10.1016/j.virusres.2007.07.012 ◽

2007 ◽

Vol 129 (2) ◽

pp. 73-79 ◽

Cited By ~ 54

Author(s):

Anna Jakubiec ◽

Isabelle Jupin

Keyword(s):

Virus Replication ◽

Rna Virus ◽

Positive Strand ◽

Positive Strand Rna Virus ◽

Positive Strand Rna

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Antiviral Innate Immune Response Interferes with the Formation of Replication-Associated Membrane Structures Induced by a Positive-Strand RNA Virus

mBio ◽

10.1128/mbio.01991-16 ◽

2016 ◽

Vol 7 (6) ◽

Cited By ~ 12

Author(s):

Diede Oudshoorn ◽

Barbara van der Hoeven ◽

Ronald W. A. L. Limpens ◽

Corrine Beugeling ◽

Eric J. Snijder ◽

...

Keyword(s):

Immune System ◽

Virus Replication ◽

Innate Immune System ◽

Rna Virus ◽

Innate Immune ◽

Membrane Structures ◽

Positive Strand ◽

Induced Membrane ◽

Positive Strand Rna Virus ◽

Positive Strand Rna

ABSTRACTInfection with nidoviruses like corona- and arteriviruses induces a reticulovesicular network of interconnected endoplasmic reticulum (ER)-derived double-membrane vesicles (DMVs) and other membrane structures. This network is thought to accommodate the viral replication machinery and protect it from innate immune detection. We hypothesized that the innate immune response has tools to counteract the formation of these virus-induced replication organelles in order to inhibit virus replication. Here we have investigated the effect of type I interferon (IFN) treatment on the formation of arterivirus-induced membrane structures. Our approach involved ectopic expression of arterivirus nonstructural proteins nsp2 and nsp3, which induce DMV formation in the absence of other viral triggers of the interferon response, such as replicating viral RNA. Thus, this setup can be used to identify immune effectors that specifically target the (formation of) virus-induced membrane structures. Using large-scale electron microscopy mosaic maps, we found that IFN-β treatment significantly reduced the formation of the membrane structures. Strikingly, we also observed abundant stretches of double-membrane sheets (a proposed intermediate of DMV formation) in IFN-β-treated samples, suggesting the disruption of DMV biogenesis. Three interferon-stimulated gene products, two of which have been reported to target the hepatitis C virus replication structures, were tested for their possible involvement, but none of them affected membrane structure formation. Our study reveals the existence of a previously unknown innate immune mechanism that antagonizes the viral hijacking of host membranes. It also provides a solid basis for further research into the poorly understood interactions between the innate immune system and virus-induced replication structures.IMPORTANCEViruses with a positive-strand RNA genome establish a membrane-associated replication organelle by hijacking and remodeling intracellular host membranes, a process deemed essential for their efficient replication. It is unknown whether the cellular innate immune system can detect and/or inhibit the formation of these membrane structures, which could be an effective mechanism to delay viral RNA replication. In this study, using an expression system that closely mimics the formation of arterivirus replication structures, we show for the first time that IFN-β treatment clearly reduces the amount of induced membrane structures. Moreover, drastic morphological changes were observed among the remaining structures, suggesting that their biogenesis was impaired. Follow-up experiments suggested that host cells contain a hitherto unknown innate antiviral mechanism, which targets this common feature of positive-strand RNA virus replication. Our study provides a strong basis for further research into the interaction of the innate immune system with membranous viral replication organelles.

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Human ACE2 receptor polymorphisms predict SARS-CoV-2 susceptibility

10.1101/2020.04.07.024752 ◽

2020 ◽

Cited By ~ 42

Author(s):

Eric W. Stawiski ◽

Devan Diwanji ◽

Kushal Suryamohan ◽

Ravi Gupta ◽

Frederic A. Fellouse ◽

...

Keyword(s):

Rna Virus ◽

Surface Protein ◽

Structural Data ◽

Host Susceptibility ◽

S Protein ◽

Host Interaction ◽

Global Pandemic ◽

History Of ◽

Positive Strand Rna Virus ◽

Positive Strand Rna

AbstractSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the cause of coronavirus disease (COVID-19) that has resulted in a global pandemic. It is a highly contagious positive strand RNA virus and its clinical presentation includes severe to critical respiratory disease that appears to be fatal in ∼3-5% of the cases. The viral spike (S) coat protein engages the human angiotensin-converting enzyme2 (ACE2) cell surface protein to invade the host cell. The SARS-CoV-2 S-protein has acquired mutations that increase its affinity to human ACE2 by ∼10-15-fold compared to SARS-CoV S-protein, making it highly infectious. In this study, we assessed if ACE2 polymorphisms might alter host susceptibility to SARS-CoV-2 by affecting the ACE2 S-protein interaction. Our comprehensive analysis of several large genomic datasets that included over 290,000 samples representing >400 population groups identified multiple ACE2 protein-altering variants, some of which mapped to the S-protein-interacting ACE2 surface. Using recently reported structural data and a recent S-protein-interacting synthetic mutant map of ACE2, we have identified natural ACE2 variants that are predicted to alter the virus-host interaction and thereby potentially alter host susceptibility. In particular, human ACE2 variants S19P, I21V, E23K, K26R, T27A, N64K, T92I, Q102P and H378R are predicted to increase susceptibility. The T92I variant, part of a consensus NxS/T N-glycosylation motif, confirmed the role of N90 glycosylation in immunity from non-human CoVs. Other ACE2 variants K31R, N33I, H34R, E35K, E37K, D38V, Y50F, N51S, M62V, K68E, F72V, Y83H, G326E, G352V, D355N, Q388L and D509Y are putative protective variants predicted to show decreased binding to SARS-CoV-2 S-protein. Overall, ACE2 variants are rare, consistent with the lack of selection pressure given the recent history of SARS-CoV epidemics, however, are likely to play an important role in altering susceptibility to CoVs.

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A positive-strand RNA virus uses alternative protein-protein interactions within a viral protease/cofactor complex to switch between RNA replication and virion morphogenesis

PLoS Pathogens ◽

10.1371/journal.ppat.1006134 ◽

2017 ◽

Vol 13 (2) ◽

pp. e1006134 ◽

Cited By ~ 9

Author(s):

Danilo Dubrau ◽

M. Alejandra Tortorici ◽

Félix A. Rey ◽

Norbert Tautz

Keyword(s):

Protein Interactions ◽

Rna Virus ◽

Rna Replication ◽

Protein Protein Interactions ◽

Viral Protease ◽

Positive Strand ◽

Alternative Protein ◽

Virion Morphogenesis ◽

Positive Strand Rna Virus ◽

Positive Strand Rna

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Cytoplasmic Localization of the ORF2 Protein of Hepatitis E Virus Is Dependent on Its Ability To Undergo Retrotranslocation from the Endoplasmic Reticulum

Journal of Virology ◽

10.1128/jvi.02039-06 ◽

2007 ◽

Vol 81 (7) ◽

pp. 3339-3345 ◽

Cited By ~ 55

Author(s):

Milan Surjit ◽

Shahid Jameel ◽

Sunil K. Lal

Keyword(s):

Endoplasmic Reticulum ◽

Hepatitis E Virus ◽

Major Capsid Protein ◽

Rna Virus ◽

Hepatitis E ◽

26S Proteasome ◽

Orf2 Protein ◽

Surface Localization ◽

Positive Strand Rna Virus ◽

Positive Strand Rna

ABSTRACT Hepatitis E virus (HEV) is a positive-strand RNA virus that is prevalent in much of the developing world. ORF2 is the major capsid protein of HEV. Although ORF2 is an N-linked glycoprotein, it is abundantly located in the cytoplasm in addition to having membrane and surface localization. The mechanism by which ORF2 protein obtains access to the cytoplasm is unknown. In this report, we prove that initially all ORF2 protein is present in the endoplasmic reticulum and a fraction of it becomes retrotranslocated to the cytoplasm. The ability of ORF2 to be retrotranslocated is dependent on its glycosylation status and follows the canonical dislocation pathway. However, in contrast to general substrates of the dislocation pathway, retrotranslocated ORF2 protein is not a substrate of the 26S proteasome complex and is readily detectable in the cytoplasm in the absence of any protease inhibitor, suggesting that the retrotranslocated protein is stable in the cytoplasm. This study thus defines the pathway by which ORF2 obtains access to the cytoplasm.

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Increase of SARS-CoV 3CL peptidase activity due to macromolecular crowding effects in the milieu composition

Biological Chemistry ◽

10.1515/bc.2010.145 ◽

2010 ◽

Vol 391 (12) ◽

Cited By ~ 10

Author(s):

Debora N. Okamoto ◽

Lilian C.G. Oliveira ◽

Marcia Y. Kondo ◽

Maria H.S. Cezari ◽

Zoltán Szeltner ◽

...

Keyword(s):

Rna Virus ◽

Antiviral Agents ◽

Fine Tuning ◽

Host Cells ◽

Respiratory Syndrome Virus ◽

Peptidase Activity ◽

Buffer Solutions ◽

Tuning Mechanism ◽

Positive Strand Rna Virus ◽

Positive Strand Rna

Abstract The 3C-like peptidase of the severe acute respiratory syndrome virus (SARS-CoV) is strictly required for viral replication, thus being a potential target for the development of antiviral agents. In contrast to monomeric picornavirus 3C peptidases, SARS-CoV 3CLpro exists in equilibrium between the monomer and dimer forms in solution, and only the dimer is proteolytically active in dilute buffer solutions. In this study, the increase of SARS-CoV 3CLpro peptidase activity in presence of kosmotropic salts and crowding agents is described. The activation followed the Hofmeister series of anions, with two orders of magnitude enhancement in the presence of Na2SO4, whereas the crowding agents polyethylene glycol and bovine serum albumin increased the hydrolytic rate up to 3 times. Kinetic determinations of the monomer dimer dissociation constant (K d) indicated that activation was a result of a more active dimer, without significant changes in K d values. The activation was found to be independent of substrate length and was derived from both k cat increase and K m decrease. The viral peptidase activation described here could be related to the crowded intracellular environment and indicates a further fine-tuning mechanism for biological control, particularly in the microenvironment of the vesicles that are induced in host cells during positive strand RNA virus infection.

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