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Вирусные детерминанты, которые движут Enterovirus-A71 фитнес и вирулентность.

Болезнь ручья, нога и мута (HFMD), как правило, является самоограничивающейся, мягкой детской болезнью, вызванной главным образом вирусом Коксаки А16 (CVA16) и Enterovirus A71 (EV-A71), которые являются членами семейства Пикорнавиридае. Однако повторяющиеся вспышки и эпидемии ГФМР в связи с инфекцией ЭВ-А71 в западной части Тихого океана и склонностью штаммов ЭВ-А71 вызывать серьезные неврологические осложнения сделали этот нейротропический вирус серьезной проблемой для здоровья населения в пострадавших странах. Высокие темпы мутации, ведущие к вирусным квазивидным явлениям в сочетании с часты

Emerging paramyxoviruses: molecular mechanisms and antiviral strategies.

In recent years, several paramyxoviruses have emerged to infect humans, including previously unidentified zoonoses. Hendra and Nipah viruses (henipaviruses within this family) were first identified in the 1990s in Australia, Malaysia and Singapore, causing epidemics with high mortality and morbidity rates in affected animals and humans. Other paramyxoviruses, such as Menangle virus, Tioman virus, human metapneumovirus and avian paramyxovirus 1, which cause less morbidity in humans, have also been recently identified. Although the Paramyxoviridae family of viruses has been previously recognised

Acquisition of specific human respiratory tract binding by 2.3.4.4b H5N1 hemagglutinins requires multiple mutations.

It has been suggested that the hemagglutinin of the human-infecting cattle-derived 2.3.4.4b virus A/Texas/34 H5N1 (H5TX) requires only one mutation, namely Q226L, to switch from binding avian-type to human-type receptor preference. In this study, we examined the binding of H5TX Q226L, along with other key mutations, to sections of human trachea. We conclude that, while H5TX Q226L can bind human-type receptors, more than a single mutation is required for this protein to bind to human respiratory tract tissue. We also report changes in receptor-binding specificity of another 2.3.4.4b HA mutant,

Insertion of host-derived costimulatory molecules CD80 (B7.1) and CD86 (B7.2) into human immunodeficiency virus type 1 affects the virus life cycle.

Human immunodeficiency virus type 1 (HIV-1) carries virus-encoded and host-derived proteins. Recent advances in the functional characterization of host molecules inserted into mature virus particles have revealed that HIV-1 biology is influenced by the acquisition of host cell membrane components. The CD28/B7 receptor/ligand system is considered one of the fundamental elements of the normal immune response. Two major cell types that harbor HIV-1 in vivo, i.e., monocytes/macrophages and CD4+ T cells, express the costimulatory molecules CD80 (B7.1) and CD86 (B7.2). We investigated whether CD80 a

Гепаран сульфат является важным посредником инфекции вируса Эбола в поляризированных эпителиальных клетках.

СПРАВОЧНАЯ ИНФОРМАЦИЯ: В настоящее время не имеется утвержденных УЛХ вакцин или методов лечения вирусного заболевания Эбола (ВИД), и терапия по-прежнему в значительной степени поддерживается. Вирус Эболы (ЭБОВ) имеет широкий тканевой тропизм и может заразить различные клетки, включая эпителиальные клетки. Эпифелевые клетки отличаются от большинства других типов клеток по их поляризованному фенотипу и функции барьера. В поляризированных клетках апичные и басоугольные мембранные области демаркируются жесткими соединениями и специализированными устройствами сортировки, что приводит к различиям в

Совпадение в аннотации оригинала
BACKGROUND: Currently, no FDA-approved vaccines or treatments are available for Ebola virus disease (EVD), and therapy remains largely suppo … n sulfate, significantly reduced cell susceptibility to basolateral infection, likely by inhibiting virus attachment. CONCLUSIONS: Our results show cell polarity has an impact on EBOV infection. EBOV preferentially infects polarized cells through the basolateral route. Access to heparan sulfate is an important factor during basolateral infection and blocking inte …

Molecular mechanisms of Japanese encephalitis virus infection and advances in vaccine research.

Japanese encephalitis (JE) is a central nervous system disease caused by the Japanese encephalitis virus (JEV), resulting in high morbidity and mortality, especially in Asia. This review summarizes the current understanding of the JEV infection cycle, including virus attachment and entry, genome replication, viral protein translation, and virus particle assembly and release. The roles of host factors and viral proteins in these processes are discussed. Furthermore, the latest advancements in JE vaccine research are emphasized, including the development of attenuated vaccine SA14-14-2, inactiva…

Structure of hepatitis E viral particle.

Hepatitis E is acute hepatitis caused by infection of hepatitis E virus (HEV) via a fecal-to-oral or zoonotic route. HEV is a small, non-enveloped virus containing positive strand RNA as a genome. Recently, the three-dimensional structures of the HEV-like particles and spike domain protruded from the surface of the particle expressed by recombinant baculovirus or bacteria have been revealed. Based on these reports, the structural features of the HEV capsid subunit and viral particle are reviewed to give insights to the mechanisms underlying the particle assembly, antigenicity, host cell attach

Peptide T does not affect induction of pineal N-acetyltransferase by vasoactive intestinal peptide.

It has been suggested that the HIV virus binds to VIP recognition sites which can be blocked by the octapeptide, peptide T. Stimulation of VIP receptors on pinealocytes activates adenylate cyclase and increases the activity of the enzyme serotonin N-acetyltransferase (NAT). We examined whether peptide T or D-Ala peptide T amide affected this induction. We found no evidence for peptide T interference with NAT induction and conclude that if peptide T inhibits attachment of HIV virus to VIP receptors, it does so at regions other than that occupied by VIP in stimulating adenylate cyclase and NAT.

Porcine reproductive and respiratory syndrome virus hijacks the non-canonical enzymatic function of PHGDH to arrest autophagic flux for viral replication.

Viruses frequently hijack host metabolic enzymes to fuel replication. However, the mechanisms underlying this hijacking and utilization of metabolic enzymes remain poorly understood. In this study, we report a sophisticated mechanism by which porcine reproductive and respiratory syndrome virus (PRRSV) exploits a non-canonical enzymatic function of PHGDH (phosphoglycerate dehydrogenase) to modulate macroautophagy/autophagy. We demonstrate that PRRSV infection recruits the transcription factor ZNF143 (zinc finger protein 143) to transcriptionally repress PHGDH expression. Importantly, the antivi

Identification of UL3.5 as a novel substrate of DPV US3 kinase whose phosphorylation at Ser64/Ser84 enhances protein stability and promotes viral release, and cell-to-cell spread.

Duck plague virus (DPV) is a major pathogen threatening waterfowl industry. As a conserved alphaherpesvirus kinase, DPV US3 participates in viral replication, while its functional substrates are largely uncharacterized. In this study, we verified that US3 directly binds and phosphorylates UL3.5 at Ser64 and Ser84. This post-translational modification inhibits protein degradation and prolongs the half-life of UL3.5. A phosphorylation-deficient recombinant virus was constructed, and phenotypic assays demonstrated that mutated virus had defective replication. Further tests indicated that UL3.5 ph

Molecular pathogenesis of Theiler's murine encephalomyelitis virus-induced demyelinating disease in mice.

After an acute phase of virus growth in neurons (e.g. anterior horn cells), Theiler's murine encephalomyelitis virus (TMEV) persists as a chronic productive infection, largely in macrophages in the CNS white matter. TMEV replication in macrophages is highly restricted, probably as the result of host cell factors. The preponderance of evidence indicates that TMEV persistence leads to immunopathologic damage of myelin, mediated by major histocompatibility class II-restricted Th1 lymphocytes directed at a virus epitope(s) rather than host neuroantigens at least early in the infection. Analysis of

Mouse adenovirus type 1 and human adenovirus type 5 differ in endothelial cell tropism and liver targeting.

BACKGROUND: For adenovirus vectors derived from human serotype 5 (Ad5), the efficiency and safety after intravascular delivery is hindered by their sequestration in nontarget tissues, predominantly the liver. The latter is largely dictated by adenovirus binding to blood coagulation zymogens. In addition, several target cells, such as endothelial and smooth muscle cells, are difficult to transduce by Ad5 due to the low expression of the primary coxsackie-adenovirus receptor (CAR). Therefore, alternative adenovirus serotypes are being explored. METHODS: In the present study, we assessed the tro

The mechanism of ribosomal recruitment during translation initiation on the Type 2 encephalomyocarditis virus IRES.

The encephalomyocarditis virus (EMCV) internal ribosomal entry side (IRES) and other Type 2 IRESs favor translation of the viral genome during infection. The domains H-L of these IRESs specifically interact with the cellular translation initiation factors eIF4G/eIF4A through their essential JK domain. However, the JK domain is not sufficient for IRES activity, which also strictly requires the preceding domain I of unknown function. To identify interactions that drive ribosomal attachment to eIF4G/eIF4A-bound Type 2 IRESs, we determined the cryo-EM structure of 48S initiation complexes formed o

Covalent functionalization of polypropylene filters with diazirine-photosensitizer conjugates producing visible light driven virus inactivating materials.

The SARS-CoV-2 pandemic has highlighted the weaknesses of relying on single-use mask and respirator personal protective equipment (PPE) and the global supply chain that supports this market. There have been no major innovations in filter technology for PPE in the past two decades. Non-woven textiles used for filtering PPE are single-use products in the healthcare environment; use and protection is focused on preventing infection from airborne or aerosolized pathogens such as Influenza A virus or SARS-CoV-2. Recently, C-H bond activation under mild and controllable conditions was reported for c

Promotion of hepatitis B virus infection by extracellular apolipoprotein E.

UNLABELLED: Chronic hepatitis B virus (HBV) infection remains a major burden to global health, affecting more than 250 million people worldwide. HBV and host interactions determine the HBV chronicity. Our previous studies have found that human apolipoprotein E (apoE) is incorporated in infectious HBV virions and plays important roles in HBV infection and morphogenesis. ApoE mediates HBV cell attachment through its interaction with cell surface receptors such as the low-density lipoprotein receptor (LDLR) family members and heparan sulfate proteoglycans (HSPGs). More importantly, both HBV-assoc

Enhanced Enterovirus D68 Replication in Neuroblastoma Cells Is Associated with a Cell Culture-Adaptive Amino Acid Substitution in VP1.

Since its emergence in the United States in 2014, enterovirus D68 (EV-D68) has been and is associated with severe respiratory diseases and acute flaccid myelitis. Even though EV-D68 has been shown to replicate in different neuronal cells in vitro, it is currently poorly understood which viral factors contribute to the ability to replicate efficiently in cells of the central nervous system and whether this feature is a clade-specific feature. Here, we determined the replication kinetics of clinical EV-D68 isolates from (sub)clades A, B1, B2, B3, and D1 in human neuroblastoma cells (SK-N-SH). Su

Influenza Virus Neuraminidase Structure and Functions.

With the constant threat of emergence of a novel influenza virus pandemic, there must be continued evaluation of the molecular mechanisms that contribute to virulence. Although the influenza A virus surface glycoprotein neuraminidase (NA) has been studied mainly in the context of its role in viral release from cells, accumulating evidence suggests it plays an important, multifunctional role in virus infection and fitness. This review investigates the various structural features of NA, linking these with functional outcomes in viral replication. The contribution of evolving NA activity to viral

Influenza hemagglutinin and neuraminidase membrane glycoproteins.

Considerable progress has been made toward understanding the structural basis of the interaction of the two major surface glycoproteins of influenza A virus with their common ligand/substrate: carbohydrate chains terminating in sialic acid. The specificity of virus attachment to target cells is mediated by hemagglutinin, which acquires characteristic changes in its receptor-binding site to switch its host from avian species to humans. Anti-influenza drugs mimic the natural sialic acid substrate of the virus neuraminidase enzyme but utilize the much tighter binding of the drugs for efficacy. Re…

Incorporation of fowl plague virus hemagglutinin into murine leukemia virus particles and analysis of the infectivity of the pseudotyped retroviruses.

We describe retrovirus particles carrying the fowl plague virus (FPV) hemagglutinin (HA). When expressed in cells providing Moloney murine l … n retroviral particles with chimeric MoMLV-derived envelope glycoproteins that efficiently retarget virus attachment but are only weakly fusogenic. Our results suggest that HA can in some cases enhance the fusion ability of these retroviral particles, depending on the cell surface molecule that is used as a receptor.

Reaction of the host to the tick-bite. II. Distribution of tick borne encephalitis virus in sucking ticks.

No reactive histological changes of the dermis and no cement cone formation were observed at the insertion site of tick mouthparts by feeding of H. inermis larvae. Conversely, cement formation was observed by feeding of H. inermis female. Fully fed D. marginatus larvae on viraemic mice showed bright fluorescence in oesophagus, suboesophageal ganglion, salivary glands, a few gut cells and in lumen of Malpighian tubuli. We consider the penetration of virus from oesophagus to suboesophageal ganglion as the possible route of primary virus infection. Sections through the D. reticulatus nymphs durin