Viral infection of cells is a highly intricate process that involves the complex virus-cell interactions. Recently, virologists can monitor the virus life cycle at the primary infection site in real-time using various virus tracking techniques. Herpesviruses, a class of large enveloped DNA viruses, are important pathogens threatening the health of humans and animals. This review discussed the applications of different virus tracking techniques in herpesvirus studies, to provide new insights into virus-cell interactions and replication mechanisms of herpesviruses. Though the techniques have widely been exploited, some issues need to be addressed, such as the selection of the optimal site to insert reporters and the inability to track the whole process of the virus life cycle. With the updated tracking techniques, hopefully, more complex replication mechanismsof herpesviruses will be revealed in detail.
Animals ; Herpesviridae ; pathogenicity ; physiology ; Humans ; Virus Diseases ; Virus Physiological Phenomena ; Virus Replication

MicroRNA (miRNA) are small non-coding molecules of ribonucleic acid. They are about 22 nucleotides in length, single-stranded, and mediate post-translational regulation by the repression or degradation of messenger RNA(mRNA). miRNA play a key part in the proliferation, differentiation and death of cells. Viral infection is one of the most common causes of human disease. Some studies have found that miRNA has a very close relationship with viral infection, which has an effect on viral replication, the immune response and antiviral immunity. Use of miRNA may become the cornerstone of new methods for the diagnosis and treatment of viral infection. This article summarizes the progress of research into miRNA and viral infection.
Animals ; Humans ; MicroRNAs ; genetics ; metabolism ; Virus Diseases ; genetics ; metabolism ; virology ; Virus Physiological Phenomena ; Virus Replication ; Viruses ; genetics

COPI is a protein complex that transports vesicles from the Golgi complex back to endoplasmic reticulum. Many viruses such as RNA viruses, DNA viruses and retroviruses, hijack or adapt COPI related proteins including coatomer, ARF1 and GBF1 for their own benefits. Here, we summarize the current progress of the roles of COPI related proteins in virus replication.
Animals ; Coat Protein Complex I ; genetics ; metabolism ; Humans ; Virus Diseases ; genetics ; metabolism ; virology ; Virus Physiological Phenomena ; Virus Replication

Phages also known as bacteria viruses, are recognized as the most abundant and diverse microbes. This diversity is adapting to the selective pressures such as the prevalence of the phage resistance mechanisms of bacteria. Phages invade and lyse bacterial through six steps (adsorption, injection, replication, transcription translation, assemble, release). Bacteria evolve to many anti-phage mechanisms to avoid phage infection and lysis. This paper focus on a variety of anti-phage mechanisms of bacteria.
Bacteria ; genetics ; virology ; Bacterial Physiological Phenomena ; Bacteriophages ; genetics ; physiology ; DNA Replication ; Evolution, Molecular ; Virus Attachment

In eukaryotic cells, multivesicular bodies (MVBs) are required for trafficking of membrane proteins to lysosomes for selective destruction. The sorting of ubiquitylated membrane proteins into multivesicular bodies and the biogenesis of MVBs are mediated by the endosomal sorting complex required for transport (ESCRT). Topologically equivalent to the budding of intralumenal vesicles from the limiting membrane of the MVBs, the ESCRT complex is also involved in cytokinetic abscission, phagophore formation, and enveloped virus budding. Many retroviruses and RNA viruses encode "late-domain" motifs that are able to interact with the components of the ESCRT complex, and the interactions recruit ESCRT-III and VPS4 to the viral assembly and budding sites. Recently, few studies revealed that the ESCRT complex is also required for efficient egress of some DNA viruses, including Hepatitis B, Herpes simplex virus type-1, and Autographa californica multiple nucleopolyhedrovirus. Further examination of virus-ESCRT interactions should shed light on the detailed mechanism of virus assembly and budding.
Endosomal Sorting Complexes Required for Transport ; physiology ; Humans ; Viral Envelope Proteins ; metabolism ; Virus Assembly ; Virus Physiological Phenomena ; Virus Release ; Viruses ; growth & development

Herpes simplex virus (HSV), including HSV-1 and HSV-2, is an important pathogen that can cause many diseases. Usually these diseases are recurrent and incurable. After lytic infection on the surface of peripheral mucosa, HSV can enter sensory neurons and establish latent infection during which viral replication ceases. Moreover, latent virus can re-enter the replication cycle by reactivation and return to peripheral tissues to start recurrent infection. This ability to escape host immune surveillance during latent infection and to spread during reactivation is a viral survival strategy and the fundamental reason why no drug can completely eradicate the virus at present. Although there are many studies on latency and reactivation of HSV, and much progress has been made, many specific mechanisms of the process remain obscure or even controversial due to the complexity of this process and the limitations of research models. This paper reviews the major results of research on HSV latency and reactivation, and discusses future research directions in this field.
Herpes Simplex ; virology ; Herpesvirus 1, Human ; physiology ; Humans ; Virus Activation ; physiology ; Virus Latency ; physiology ; Virus Replication

Epstein-Barr virus (EBV) infection occurs by distinct mechanisms across different cell types. EBV infection of B cells in vitro minimally requires 5 viral glycoproteins and 2 cellular proteins. By contrast, infection of epithelial cells requires a minimum of 3 viral glycoproteins, which are capable of interacting with one or more of 3 different cellular proteins. The full complement of proteins involved in entry into all cell types capable of being infected in vivo is unknown. This review discusses the events that occur when the virus is delivered into the cytoplasm of a cell, the players known to be involved in these events, and the ways in which these players are thought to function.
B-Lymphocytes ; Epithelial Cells ; Epstein-Barr Virus Infections ; Herpesvirus 4, Human ; Viral Proteins ; Virus Physiological Phenomena

Coxsackievirus B3 (CVB3) is the nonenveloped virus containing a single-stranded positive-sense RNA as a genome. CVB3 infection can induce acute myocarditis and dilated cardiomypathy. CVB3 of icosahedral symmetry has four capsid proteins called VP1, VP2, VP3, and VP4. Although VP1 is a major antigenic determinant, VP2 is also an important protein for viral physiology, such as maturation cleavage and attenuation. However, VP2 study has been hampered, partly because VP2 antibody is not available. In this study, we developed peptide-based polyclonal VP2 antibody and analyzed its potency by Western blotting analysis and immunofluorescent assay. Purified B3-1 antibody (VP2 peptide antibody developed in here) showed the sensitivity and specificity, similar to VP1 monoclonal antibody which is commercially available. Moreover, this peptide antibody may be useful for double-staining with other antibodies derived from mouse. Therefore, the VP2 antibody may allow us to study CVB assembly and understand VP2 function in depth.
Animals ; Antibodies ; Blotting, Western ; Capsid Proteins ; Genome ; Mice ; Myocarditis ; RNA ; Sensitivity and Specificity ; Virus Physiological Phenomena

Enterovirus 71 is a neuroinvasive virus that is associated with severe neurological complications. We had earlier suggested that the replication capacity of a severe strain was higher than that of a mild strain. The recombinant 3CRV and 3CDRV virus strains were successfully rescued in our previous study. In the present study, we found no difference in virulence between 3CRV and severe strains. However, the capacity of replication and to cause cell injury of 3CDRV strain decreased in vitro, especially at 39.5 °C. Replacement of 3CD region in the severe strain led to milder symptoms, less body weight loss, and lower viral load in ICR mice. Histopathological findings indicated less severe injury in mice infected with 3CDRV strain. This study suggests that the 3CD region contributes to the attenuation of the severe strain, including its replication capacity and temperature sensitivity.
Animals ; Cytopathogenic Effect, Viral ; Enterovirus A, Human ; genetics ; pathogenicity ; Enterovirus Infections ; pathology ; virology ; Gene Expression Regulation, Viral ; Mice ; Mice, Inbred ICR ; Mutation ; Viral Load ; Viral Proteins ; genetics ; metabolism ; Virulence ; Virus Replication

The innate immune system is essential for the initial detection of invading viruses and subsequent activation of adaptive immunity. Three types pattern recognition receptors (PRRs) in innate immune cells play a pivotal role in the first line of host defense system. PRRs include Toll-like receptors (TLRs), RIG-I-like receptors(RLRs) and nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs). PRRs recognize pathogen-associated molecular patterns(PAMPs) or danger-associated molecular patterns (DAMPs) to initiate and regulate innate and adaptive immune responses. Three types PRRs have their own features in ligand recognition and cellular location. Activated PRRs deliver signals to adaptor molecules (MyD88, TRIF, IRAK, IPS-1), which act as important messengers to activate downstream kinases (IKK complex, MAPKs, TBK1, RIP-1) and transcription factors (NF-kappaB, AP-1, IRF3), which produce effected molecules including cytokines, chemokines, inflammatory enzymes, and type I interferons. This review focuses on discussing PRRs signaling pathways and achievements in this field in order to provide beneficial strategies for human life and immune diseases prevention.
Animals ; Humans ; Immunity, Innate ; Receptors, Pattern Recognition ; genetics ; immunology ; metabolism ; Signal Transduction ; Virus Diseases ; immunology ; metabolism ; virology ; Virus Physiological Phenomena