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Alkhumra Hemorrhagic Fever Virus (AHFV): A Concise Overview.

Alkhumra fever is a viral disease caused by the Alkhumra hemorrhagic fever virus (AHFV). It belongs to family Flaviviridae, genus Flavivirus. AHFV is primarily transmitted to humans through the bite of infected ticks, for example, Hyalomma. This disease was first identified in the Kingdom of Saudi Arabia (KSA) in 1995 and then reported in other countries of the Arabian Peninsula and the Middle East. The AHFV genome consists of a positive-sense, single-stranded RNA molecule of approximately 10.2 kilobases (kb) in length. The Open Reading Frame (ORF) encodes a polyprotein precursor that is proce

Proteomics computational analyses suggest that the carboxyl terminal glycoproteins of Bunyaviruses are class II viral fusion protein (beta-penetrenes).

The Bunyaviridae family of enveloped RNA viruses includes five genuses, orthobunyaviruses, hantaviruses, phleboviruses, nairoviruses and tospoviruses. It has not been determined which Bunyavirus protein mediates virion:cell membrane fusion. Class II viral fusion proteins (beta-penetrenes), encoded by members of the Alphaviridae and Flaviviridae, are comprised of three antiparallel beta sheet domains with an internal fusion peptide located at the end of domain II. Proteomics computational analyses indicate that the carboxyl terminal glycoprotein (Gc) encoded by Sandfly fever virus (SAN), a phle

Japanese encephalitis virus NS1 and NS4B synergistically target TLR3 signaling to promote viral replication.

UNLABELLED: To establish effective infection, viral pathogens employ diverse strategies through encoded proteins to interfere with host antiviral responses. While previous studies have predominantly focused on elucidating the mechanisms by which individual viral proteins regulate type I interferon (IFN) responses, this study presents the first demonstration that Japanese encephalitis virus (JEV)-encoded NS1 and NS4B proteins cooperatively target the TLR3 receptor signaling pathway to suppress IFN production. Here, we first discovered JEV-encoded multifunctional glycoprotein NS1, which inhibits

Dengue protease-mediated activation and polarization of macrophages.

Structural proteins of viruses are well recognized as major determinants of host immune responses. However, increasing evidence indicates that viral non-structural proteins can also be released from infected cells under inflammatory conditions, including via extracellular vesicles and inflammasome-associated cell death. The immunological consequences of such extracellular exposure of viral non-structural proteins remain poorly understood. Here, we investigated a non-canonical extracellular function of the dengue virus NS2B/NS3 protease and examined its ability to modulate macrophage activation

Viroporins: emerging viral infection mechanisms and therapeutic targets.

Viroporins, virus-encoded small hydrophobic proteins, are involved in critical steps of viral infections by modulating ion homeostasis, disrupting host membrane integrity, and orchestrating key stages of the virus life cycle-from entry and replication to release. Beyond facilitating viral propagation, these pore-forming proteins exacerbate pathogenesis by disrupting cellular ion homeostasis and triggering proinflammatory responses through NLRP3 inflammasome activation. Their dual role in viral fitness and immunopathology positions viroporins as promising antiviral targets for dual-action thera

Влияние белков до мембраны и конвертов на структуру, патогенность и трпизм вируса энцефалита, переносимого клещами.

Вирус энцефалита (TBEV) — нейротропический аромат, который ежегодно вызывает тысячи человеческих инфекций. Вирусный тропизм в мозгу определяется наличием необходимых рецепторов, вводными факторами и способностью вируса преодолевать защиту хост-компьютера. Виртуальные структурные белки, предмембран (prM) и конверт (E) играют важную роль в связывании рецепторов, синтезе мембраны, созревании частиц и нейтрализации антител. Чтобы понять, как эти белки влияют на распространение вируса и тропизм в мозгу, мы создали химериковый вирус, прикрывающий ПРМ и эктодомен Е от ТБЭВ на фоне низкопатогенного ви

Совпадение в аннотации оригинала
UNLABELLED: Tick-borne encephalitis virus (TBEV) is a neurotropic flavivirus that causes thousands of human infections annually. Viral tropism in the brain is determined by the presence of necessary receptors, entry factors, and the ability of the virus to overcome host defenses. The viral structural proteins, pre-membrane (prM), and envelope (E) play an imp…

Construction and application of chimeric virus-like particles of tick-borne encephalitis virus and mosquito-borne Japanese encephalitis virus.

We have previously reported a system for packaging tick-borne encephalitis (TBE) virus subgenomic replicon RNAs into single-round infectious virus-like particles (VLPs) by using in trans expression of viral C/prM/E structural proteins. In this study, the trans-packaging system was applied to the generation of chimeric VLPs with mosquito-borne Japanese encephalitis (JE) virus. Although trans-expression of TBE virus C and JE virus prM/E proteins resulted in the secretion of VLPs, the expression of JE virus C/prM/E proteins did not lead to the secretion of VLPs, suggesting that homologous interac

The human rhinovirus: human-pathological impact, mechanisms of antirhinoviral agents, and strategies for their discovery.

As the major etiological agent of the common cold, human rhinoviruses (HRV) cause millions of lost working and school days annually. Moreover, clinical studies proved an association between harmless upper respiratory tract infections and more severe diseases e.g. sinusitis, asthma, and chronic obstructive pulmonary disease. Both the medicinal and socio-economic impact of HRV infections and the lack of antiviral drugs substantiate the need for intensive antiviral research. A common structural feature of the approximately 100 HRV serotypes is the icosahedrally shaped capsid formed by 60 identica

Protein Set Transformer: a protein-based genome language model to power high-diversity viromics.

Exponential increases in microbial and viral genomic data demand transformational advances in scalable, generalizable frameworks for their interpretation. Standard homology-based functional analyses are hindered by the rapid divergence of microbial and especially viral genomes and proteins that significantly decreases the volume of usable data. Here, we present Protein Set Transformer (PST), a protein-based genome language model that models genomes as sets of proteins without considering sparsely available functional labels. Trained on >100k viruses, PST outperforms other homology- and languag

Coronavirus nucleocapsid proteins: a multifaceted modulator in the innate immune evasion.

Coronaviruses are capable of inducing diverse infectious diseases that pose significant threats to the public health and the economic development. With a single positive-stranded RNA genome, coronaviruses utilize viral proteins to execute diverse immune escape strategies to facilitate their replication. Of all the identified structural proteins and non-structural proteins within the coronaviruses, nucleocapsid (N) protein is highly conserved and is the most abundant viral protein in infected host cells. N protein regulates the more complex and diverse mechanisms through which viruses suppress

Negative and ambisense RNA virus ribonucleocapsids: more than protective armor.

Negative and ambisense RNA viruses are the causative agents of important human diseases such as influenza, measles, Lassa fever, and Ebola hemorrhagic fever. The viral genome of these RNA viruses consists of one or more single-stranded RNA molecules that are encapsidated by viral nucleocapsid proteins to form a ribonucleoprotein complex (RNP). This RNP acts as protection, as a scaffold for RNA folding, and as the context for viral replication and transcription by a viral RNA polymerase. However, the roles of the viral nucleoproteins extend beyond these functions during the viral infection cycl

Porcine epidemic diarrhea virus: Molecular mechanisms of attenuation and vaccines.

Porcine epidemic diarrhea virus (PEDV) causes an emerging and re-emerging coronavirus disease characterized by vomiting, acute diarrhea, dehydration, and up to 100% mortality in neonatal suckling piglets, leading to huge economic losses in the global swine industry. Vaccination remains the most promising and effective way to prevent and control PEDV. However, effective vaccines for PEDV are still under development. Understanding the genomic structure and function of PEDV and the influence of the viral components on innate immunity is essential for developing effective vaccines. In the current

DNA vaccine expressing the non-structural proteins of Piscine orthoreovirus delay the kinetics of PRV infection and induces moderate protection against heart -and skeletal muscle inflammation in Atlantic salmon (Salmo salar).

Piscine orthoreovirus (PRV) causes heart- and skeletal muscle inflammation (HSMI) in farmed Atlantic salmon (Salmo salar). Erythrocytes are the main target cells for PRV. HSMI causes significant economic losses to the salmon aquaculture industry, and there is currently no vaccine available. PRV replicates and assembles within cytoplasmic structures called viral factories, mainly organized by the non-structural viral protein µNS. In two experimental vaccination trials in Atlantic salmon, using DNA vaccines expressing different combinations of PRV proteins, we found that expression of the non-st

Recent advances in discovery and functional analysis of the small proteins and microRNA expressed by polyomaviruses.

The polyomavirus family consists of a highly diverse group of small DNA viruses isolated from various species, including humans. Some family members have been used as model systems to understand the fundamentals of modern biology. After the discovery of the first two human polyomaviruses (JC virus and BK virus) during the early 1970s, their current number reached 14 today. Some family members cause considerably severe human diseases, including polyomavirus-associated nephropathy (PVAN), progressive multifocal leukoencephalopathy (PML), trichodysplasia spinulosa (TS) and Merkel cell carcinoma (

Mass spectrometry-based proteomic analysis of potential infectious bursal disease virus VP3-interacting proteins in chicken embryo fibroblasts cells.

The structural protein VP3 of infectious bursal disease virus (IBDV) plays a critical role in viral assembly, replication, immune escape, and anti-apoptosis. Interaction between VP3 and host protein factors can affect stages in the viral replication cycle. In this study, 137 host proteins interacting with VP3 protein were screened through liquid chromatography-tandem mass spectrometry (LC-MS/MS)-based proteomics approach. The functions and relevance of the proteins were obtained through bioinformatics analysis. Most VP3-interacting proteins were linked to binding, catalytic activity, and struc

Tick-borne flaviviruses alter membrane structure and replicate in dendrites of primary mouse neuronal cultures.

Neurological diseases caused by encephalitic flaviviruses are severe and associated with high levels of mortality. However, detailed mechani … n of viral antigen in the neuronal dendrites to a greater extent than infection with other viruses. Viral structural proteins, non-structural proteins and dsRNA were detected in regions in which viral antigens accumulated in dendrites after TBEV replication. Replication of a TBEV replicon after infection with virus-like particles of TBEV also induced antigen accumulation, …

Exogenous Rubella Virus Capsid Proteins Enhance Virus Genome Replication.

Enhanced replication of rubella virus (RuV) and replicons by de novo synthesized viral structural proteins has been previously described. Such enhancement can occur by viral capsid proteins (CP) alone in trans. It is not clear whether the CP in the virus particles, i.e., the exogenous CP, modulate viral genome replication. In this study, we found that exogenous RuV CP also enhanced viral genome replication, either when used to package replicons or when mixed with RNA during transfection. We demonstrated that CP does not affect the translation efficiency from genomic (gRNA) or subgenomic RNA (s…

Theiler's murine encephalomyelitis virus 3D RNA polymerase: its expression in the CNS and the specific immune response generated in persistently infected mice.

Intracerebral inoculation of the neurotropic murine picornavirus, Theiler's murine encephalomyelitis virus (TMEV), results either in an acut … n, very few cells were found to express the polymerase while many more cells showed the presence of viral structural proteins. This suggests that a restriction in viral replication, possibly at the level of polymerase expression, may be a feature of the persistent infection. However, enough polymerase was expressed to maintain a polymerase-specific antibody response in a n …

Formation of adenovirus DNA replication compartments and viral DNA accumulation sites by host chromatin regulatory proteins including NPM1.

The adenovirus (Ad) genome is believed to be packaged into the virion by forming a chromatin-like structure. The replicated viral genome is likely to be condensed through binding with viral core proteins before encapsidation. Replicated viral genomes accumulate in the central region of the nucleus, which we termed virus-induced postreplication (ViPR) body. However, the molecular mechanism by which the nuclear structure is reorganized and its functional significance in virus production are currently not understood. In this study, we found that viral packaging protein IVa2, but not capsid protei

How SARS-CoV-2 dodges immune surveillance and facilitates infection: an analytical review.

INTRODUCTION: Effective treatments for the ongoing severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic are limited. The virus has evolved strategies to evade the immune system or hijack immune responses to facilitate infection and escape immune surveillance. Mechanistically, SARS-CoV-2 takes advantage of TLR4 and cytokine-induced integrins to promote its entrance into the cell. Furthermore, the activation of pattern recognition receptors (PRR)-mediated signaling pathways is compromised by SARS-CoV-2 non-structural proteins (NSPs), accessory protein open reading frames (ORFs),