Pathogenesis Of Virus Infection Research Articles

Pathogenetic aspects of rabbits’ experimental infection caused by bovine leukemia virus

Bovine leukemia virus (BLV) is an infectious disease of cattle, causing high economic losses worldwide, especially in the field of dairy farming. There is no common vision on the problem of interspecies transmission of BLV. Therefore, a detailed study of the etiologic relationship between leukemia in cattle and other animal species is relevant. Various laboratory animal models provide insight into the pathogenesis of viral infections. The article presents the research results of two series rabbits’ intravenous infection with bovine leukemia virus (BLV) using the culture antigen FLK-BLV and the blood of rabbits with clinical, hematological and immunological signs of viral tumor growth. Blood from all animals was taken from the ear vein after 14, 21, 30 days, and then monthly for six months: to study the morphological parameters of blood and to determine the titer of antibodies to BLV. Blood serum for the presence of antibodies to BLV was examined using a diagnostic kit for the indication of animals infected with the leukemia virus in an immunodiffusion reaction produced by LLC “SRE Veterinary Medicine”, Kharkiv. It was found that the stage of the BLV provirus in the blood leukogram of infected animals was characterized by pronounced lymphocytosis on the 21st day of the experiment. The highest concentration of antibodies to BLV in the blood serum was found on the 90th day after the administration of the virus-containing material, which disappeared from the blood on the 150–180th day after infection. In experimental rabbits, after five months for thirty days, in the absence of antibodies to leukemia in the blood serum, multiple tumors of a dense consistency began to develop throughout the body. Such clinical signs and changes in the of rabbits’ blood of the experimental group are characteristic of serologically positive cows on the hematological development stage of leukemic process and correlate with the results of domestic and foreign authors. The presence of a large number of lymphoblasts, as well as leukolysis cells, in the histological preparation of lymph nodes, lungs, heart and the accumulation of lymphocytes’ immature forms around the interlobular vessels of the liver, which were found in pathohistological studies of the experimental rabbits’ organs, may indicate the development of the leukemia process on early stage in them. The results obtained indicate the ability of BLV to overcome successfully the interspecies barrier upon parenteral ingestion of heterologous individuals from infected lymphocytes and in the form of a culture antigen.

ROLE OF MODERN TECHNOLOGY FOR TREATMENT OF HCV

HCV is the main reason of the liver disease and worldwide it is one of the major issues of health due to its development into cirrhosis, failure and cancer of liver. The transference of HCV is mainly through the parental but people who use drug like intravenous are also at greatest threat. The life cycle of HCV is now understood in a more precise way due to extensive studies. Due to more understanding of this virus there is establishment of more effectual antiviral medications and also diagnostic devices. Test of nucleic acids are suggested for the validation of active HCV. Serology tests are suggested for the groups that are at the greatest risk. Earlier for the standard medications of HCV interferon (IFN-a) and ribavirin are used. Later FDA approved a number of drugs such as harvoni, simeprevir and boceprevir etc. for the proper treatment of HCV. Antiviral medications will be utilized to treat the infections of HCV. In the management of certain severe viral infection, therapeutic option has improved in a better way. There is need of follow-up and careful consideration as well as there are many new technologies that have developed for the quantitative measurement of viral genome concentration in the body fluid of patients. Initially this measurement led to important insight in the viral infection pathogenesis as well as these test also revolutionized natural history of HCV. In addition viral load test are pure tool for research, these are used in routine viral diagnosis. Viral load test are used in clinical virology for diagnosis and prognosis of patient’s.

Tetracycline and viruses: a possible treatment for COVID-19?

Tetracyclines have been used to treat many bacterial infections. The use of these antibiotics for the treatment of viral diseases dates to the 1960s to 1970s. Over the decades, the effect of tetracyclines on the pathogenesis of viral infections has been demonstrated both clinically and experimentally. Tetracyclines can act on viral infections either through their antibacterial properties or through direct antiviral action. This review focuses on clinical and experimental data that support the use of tetracycline in treating viral infections and highlights an important approach to slowing disease progression during viral infections. Tetracycline treatment might represent a strategy for eliminating the infection or inhibiting the progression of COVID-19.

Extracellular Vesicles in the Pathogenesis of Viral Infections in Humans.

Most cells can release extracellular vesicles (EVs), membrane vesicles containing various proteins, nucleic acids, enzymes, and signaling molecules. The exchange of EVs between cells facilitates intercellular communication, amplification of cellular responses, immune response modulation, and perhaps alterations in viral pathogenicity. EVs serve a dual role in inhibiting or enhancing viral infection and pathogenesis. This review examines the current literature on EVs to explore the complex role of EVs in the enhancement, inhibition, and potential use as a nanotherapeutic against clinically relevant viruses, focusing on neurotropic viruses: Zika virus (ZIKV) and human immunodeficiency virus (HIV). Overall, this review’s scope will elaborate on EV-based mechanisms, which impact viral pathogenicity, facilitate viral spread, and modulate antiviral immune responses.

Potential Therapeutic Roles for Direct Factor Xa Inhibitors in Coronavirus Infections.

Human factor Xa (FXa) is a serine protease of the common coagulation pathway. FXa is known to activate prothrombin to thrombin, which eventually leads to the formation of cross-linked blood clots. While this process is important in maintaining hemostasis, excessive thrombin generation results in a host of thrombotic conditions. FXa has also been linked to inflammation via protease-activated receptors. Together, coagulopathy and inflammation have been implicated in the pathogenesis of viral infections, including the current coronavirus pandemic. Direct FXa inhibitors have been shown to possess anti-inflammatory and antiviral effects, in addition to their established anticoagulant activity. This review summarizes the pharmacological activities of direct FXa inhibitors, their pharmacokinetics, potential drug–drug interactions and adverse effects, and the details of clinical trials involving direct FXa inhibitors in coronavirus disease 2019 (COVID-19) patients.

Correlation between premorbid IL-6 levels and COVID-19 mortality: Potential role for Vitamin D

There is recent evidence that interleukin-6 (IL-6) levels are elevated in cases of complicated COVID-19, but it is also possible that this cytokine may have a far more important role in the pathogenesis of viral infection. IL-6 is known to be modulated by Vitamin D, and there is preliminary evidence that deficiency of this vitamin is linked to poorer outcomes. To identify whether IL-6 levels prior to infection might predict outcome, early data on COVID-19 mortality from Italy and the UK were compared with previously published results of mean IL-6 levels from these countries as well as from the USA. There was a highly significant correlation (r = 0.9883; p = 0.00025) between age-stratified mortality rates and IL-6 levels from previously published data on healthy individuals. To determine whether Vitamin D may be beneficial at lowering IL-6 levels in patients, a limited analysis of trials examining the relationship between these entities published since 2015 was undertaken. Eight out of 11 studies described a significant lowering effect of Vitamin D on IL-6. Given that IL-6 likely facilitates viral cell entry and replication, levels prior to infection may predict mortality. This provides a rationale for prophylactic and therapeutic measures directed at lowering IL-6, including Vitamin D prescription.

COVID-19, neutrophil extracellular traps and vascular complications in obstetric practice.

An issue of the novel coronavirus infection spreading is currently in the first place among others in the list of the international medical community. Due to lack of information, conflicting research findings, multicomponent effect of the virus on the body host, as well as various consequences that the virus triggers in the body, now every medical specialty does study the viral attack pathogenesis. Recent months showed that vascular complications are the most severe in the Coronavirus Disease 2019 (COVID-19) and are the main cause of death in the patients. The mechanisms of vascular complications are complex and affect both the hemostatic system and immune responses, "inflammatory storm", disorders of the renin-angiotensin-aldosterone system, endotheliopathy, etc. Due to the leading role of vascular complications in the viral infection pathogenesis, several groups of patients are at extra risk, including pregnant women, patients with a burdened obstetric history, with hereditary thrombophilia and antiphospholipid syndrome, and patients after in vitro fertilization (IVF). In this category of pregnant women, use of low-molecular-weight heparins (LMWH) is particularly important for both prevention of vascular and obstetric complications, and for pathogenetic therapy of COVID-19.

Hsp70 Is a Potential Therapeutic Target for Echovirus 9 Infection.

Echovirus is an important cause of viral pneumonia and encephalitis in infants, neonates, and young children worldwide. However, the exact mechanism of its pathogenesis is still not well understood. Here, we established an echovirus type 9 infection mice model, and performed two-dimensional gel electrophoresis (2DE) and tandem mass spectrometry (MS/MS)-based comparative proteomics analysis to investigate the differentially expressed host proteins in mice brain. A total of 21 differentially expressed proteins were identified by MS/MS. The annotation of the differentially expressed proteins by function using the UniProt and GO databases identified one viral protein (5%), seven cytoskeletal proteins (33%), six macromolecular biosynthesis and metabolism proteins (28%), two stress response and chaperone binding proteins (9%), and five other cellular proteins (25%). The subcellular locations of these proteins were mainly found in the cytoskeleton, cytoplasm, nucleus, mitochondria, and Golgi apparatus. The protein expression profiles and the results of quantitative RT-PCR in the detection of gene transcripts were found to complement each other. The differential protein interaction network was predicted using the STRING database. Of the identified proteins, heat shock protein 70 (Hsp70), showing consistent results in the proteomics and transcriptomic analyses, was analyzed through Western blotting to verify the reliability of differential protein expression data in this study. Further, evaluation of the function of Hsp70 using siRNA and quercetin, an inhibitor of Hsp70, showed that Hsp70 was necessary for the infection of echovirus type 9. This study revealed that echovirus infection could cause the differential expression of a series of host proteins, which is helpful to reveal the pathogenesis of viral infection and identify therapeutic drug targets. Additionally, our results suggest that Hsp70 could be a useful therapeutic host protein target for echovirus infection.

Importance of Epstein–Barr virus infection in pathogenesis of proliferative complications in children with endogenous uveitis

Endogenous uveitis (EU) in children is a multifactorial sight-threatening disease that reduces patient’s quality of life. Proliferative syndrome (PS) coupled to developing adhesions, opacity of vitreous body, epiretinal and preretinal membranes is one of the most serious EU complications, with yet-unknown pathogenesis. Among the numerous trigger factors, a role for infections, particularly human herpes group-driven, is proposed. The goal of the study was to assess a potential role of Herpes simplex viruses type 1 (HSV-1), Herpes simplex viruses type 2 (HSV-2), Epstein–Barr virus (EBV) and Cytomegalovirus (CMV) played in the PS pathogenesis in children with endogenous uveitis. 112 patients aged 3–17 years (mean age 10 years) with (93 patients)/without PS (19 children) were examined. IgM and IgG antibodies (markers of chronic and active infection) against HSV-1/2, EBV and CMV were detected by ELISA. A significantly increased PS rate in infected vs. uninfected children was revealed solely for EBV infection (p = 0.03), but not for HSV-1/2 (p 0.05) or CMV-positive patients (p 0.05). However, PS emergence in EBV-negative patients also suggests that some factors might contribute to proliferation in intraocular inflammation. In addition, level of serum IL-8 and IL-6 were assessed by multiplex analysis in 28 children. It was found that IL-8 was detected in all patients, with great individual fluctuations (5.6–2743 pg/ml). Enhanced systemic IL-8 level tended to rise in patients with more prominent proliferation and serological markers of EBV reactivation. However, serum IL-6 was detected by about 2-fold less often reaching up to 55% cases (variation of individual indices 1.3–35.5 pg/ml). A correlation between PS severity, EBV infection activity and systemic IL-6 level was not observed. Further studies evaluating a role of EBV infection in PS pathogenesis pediatric endogenous uveitis are necessary, as it may underlie a rationale for including antiherpetic drugs into a combination therapy.

Platelet-endothelial associations may promote cytomegalovirus replication in the salivary gland in mice

Platelet decline is a feature of many acute viral infections, including cytomegalovirus (CMV) infection in humans and mice. Platelet sequestration in association with other cells, including endothelium and circulating leukocytes, can contribute to this decline and influence the immune response to and pathogenesis of viral infection. We sought to determine if platelet-endothelial associations (PEAs) contribute to platelet decline during acute murine CMV (mCMV) infection, and if these associations affect viral load and production. Male BALB/c mice were infected with mCMV (Smith strain), euthanized at timepoints throughout acute infection and compared to uninfected controls. An increase in PEA formation was confirmed in the salivary gland at all post-inoculation timepoints using immunohistochemistry for CD41+ platelets co-localizing with CD34+ vessels. Platelet depletion did not change amount of viral DNA or timecourse of infection, as measured by qPCR. However, platelet depletion reduced viral titer of mCMV in the salivary glands while undepleted controls demonstrated robust replication in the tissue by plaque assay. Thus, platelet associations with endothelium may enhance the ability of mCMV to replicate within the salivary gland. Further work is needed to determine the mechanisms behind this effect and if pharmacologic inhibition of PEAs may reduce CMV production in acutely infected patients.

Blocking cellular N-glycosylation suppresses human cytomegalovirus entry in human fibroblasts

N-glycosylation plays an important role in the pathogenesis of viral infections. However, the role of host cell N-glycosylation in human cytomegalovirus (hCMV) infection remains to be elucidated. In this study, we found that blocking or removal of cellular N-glycosylation by tunicamycin, peptide-N-glycosidase F (PNGase F) treatment, or N-acetylglucosaminyltransferase I (MGAT1) knockdown resulted in suppression of hCMV infection in human fibroblasts. This suppression was reversed following N-glycosylation restoration. Immunofluorescence and flow cytometry analysis showed that blockade of cellular N-glycosylation interfered with hCMV entry rather than binding. Removal of N-glycosylation on epidermal growth factor (EGFR) and integrin β3, two proposed hCMV receptors, blocked their interaction with hCMV glycoproteins B and H. It also suppressed activation of these receptors and downstream integrin β3/Src signaling. Taken together, these results suggest that N-glycosylation of host cell glycoproteins including two proposed hCMV receptors is critical for hCMV entry rather than attachment. They provide novel insights into the biological process important for the early stage of hCMV infection with potential therapeutic implications.

Experimental infection of sheep with Bovine leukemia virus (BLV): Minimum dose of BLV-FLK cells and cell-free BLV and neutralization activity of natural antibodies

Bovine leukemia virus (BLV) is an important cattle pathogen that causes major economic losses worldwide, especially in dairy farms. The use of animal models provides valuable insight into the pathogenesis of viral infections. Experimental infections of sheep have been conducted using blood from BLV-infected cattle, infectious BLV molecular clones or tumor-derived cells. The Fetal Lamb Kidney cell line, persistently infected with BLV (FLK-BLV), is one of the most commonly used long-term culture available for the permanent production of virus. FLK-BLV cells or the viral particles obtained from the cell-free culture supernatant could be used as a source of provirus or virus to experimentally infect sheep. In this report, we aimed to determine the minimum amount of FLK-BLV cells or cell-free supernatant containing BLV needed to produce infection in sheep. We also evaluated the amount of antibodies obtained from a naturally-infected cow required to neutralize this infection. We observed that both sheep experimentally inoculated with 5000 FLK-BLV cells became infected, as well as one of the sheep receiving 500 FLK-BLV cells. None of the animals inoculated with 50 FLK-BLV cells showed evidence of infection. The cell-free FLK-BLV supernatant proved to be infective in sheep up to a 1:1000 dilution. Specific BLV antibodies showed neutralizing activity as none of the sheep became infected. Conversely, the animals receiving a BLV-negative serum showed signs of BLV infection. These results contribute to the optimization of a sheep bioassay which could be useful to further characterize BLV infection.

IFITM Genes, Variants, and Their Roles in the Control and Pathogenesis of Viral Infections.

Interferon-induced transmembrane proteins (IFITMs) are a family of small proteins that localize in the plasma and endolysosomal membranes. IFITMs not only inhibit viral entry into host cells by interrupting the membrane fusion between viral envelope and cellular membranes, but also reduce the production of infectious virions or infectivity of progeny virions. Not surprisingly, some viruses can evade the restriction of IFITMs and even hijack the antiviral proteins to facilitate their infectious entry into host cells or promote the assembly of virions, presumably by modulating membrane fusion. Similar to many other host defense genes that evolve under the selective pressure of microorganism infection, IFITM genes evolved in an accelerated speed in vertebrates and many single-nucleotide polymorphisms (SNPs) have been identified in the human population, some of which have been associated with severity and prognosis of viral infection (e.g., influenza A virus). Here, we review the function and potential impact of genetic variation for IFITM restriction of viral infections. Continuing research efforts are required to decipher the molecular mechanism underlying the complicated interaction among IFITMs and viruses in an effort to determine their pathobiological roles in the context of viral infections in vivo.

Methods for characterizing protein acetylation during viral infection.

Lysine acetylation is a prevalent posttranslational modification that acts as a regulator of protein function, subcellular localization, and interactions. A growing body of work has highlighted the importance of temporal alterations in protein acetylation during infection with a range of human viruses. It has become clear that both cellular and viral proteins are decorated by lysine acetylations, and that these modifications contribute to core host defense and virus replication processes. Further defining the extent and dynamics of protein acetylation events during the progression of an infection can provide an important new perspective on the intricate mechanisms underlying the biology and pathogenesis of virus infections. Here, we provide protocols for identifying, quantifying, and probing the regulation of lysine acetylations during viral infection. We describe the use of acetyl-lysine immunoaffinity purification and quantitative mass spectrometry for assessing the cellular acetylome at different stages of an infection. As an alternative to traditional antibody-mediated western blotting, we discuss the benefits of targeted mass spectrometry approaches for detecting and quantifying site-specific acetylations on proteins of interest. Specifically, we provide a protocol using parallel reaction monitoring (PRM). We further discuss experimental considerations that are specific to studying viral infections. Finally, we provide a brief overview of the types of assays that can be employed to characterize the function of an acetylation event in the context of infection. As a method to interrogate the regulation of acetylation, we describe the Fluor de Lys assay for monitoring the enzymatic activities of deacetylases.

Assessment of hepatitis B virus genotype D and interleukin-10, interferon gamma, and tumor necrosis factor-α in fulminant hepatic failure

Background: Genotypically, hepatitis B virus (HBV) is divided into 8 groups, A–H. The interaction between HBV replication and immune responses against HBV infection plays an important role in the pathogenesis of virus infection. Aims and Objectives: In an attempt to elucidate the role of immunomodulatory, pro-inflammatory, and anti-inflammatory mediators in the pathogenesis of HBV genotype D fulminant hepatitis (FH), we assessed the role of interferon gamma (IFN-γ), tumor necrosis factor-α (TNF-α), and interleukin-10 (IL-10) in such patients. Subjects and Methods: Two hundred and seventy-six cases of acute hepatitis among which 37 cases of fulminant hepatic failure were screened. A genotyping system based on polymerase chain reaction using type-specific primers was used in this study (Sami et al. 2013). TNF-α, IL-10 levels, and IFN-γ serum level were measured by ELISA. Results: Genotype D was detected in 10 cases (27.02%) out of 37 FH patients. Mean IL-10, IFN-γ, and TNF-α levels in FH patients were significantly higher than the healthy controls at 127.6 ± 73.45 pg/ml (P

Cyclophilins: The Structure and Functions of an Important Peptidyl-prolyl Isomerase

Cyclophilins are a subgroup of highly conserved protein family immunophilins which are peptidyl-prolyl isomerases that interconvert between the cis and trans positions. They can act as chaperones in maintaining conformational quality control of proteomes. They are structurally conserved throughout evolution and have been found in mammals, plants, insects, fungi, and bacteria. They share a common fold architecture consisting of 8 antiparallel beta sheets and two alpha helices that pack against the sheets. They exist in the cellular compartment of most tissues and encode special functions. Intracellular Cyclophilins are secreted from cells in response to inflammatory stimuli and can mediate intercellular communication. Pro-inflammatory signals may be stimulated by extracellular Cyclophilin. Overexpression of Cyclophilins can contribute to pathological conditions. Cyclophilins are involved in the pathogenesis of viral infection, neurodegenerative diseases, ageing and cancer. Exhibiting several molecular functions, Cyclophilins can bind to cyclosporine and calcium-dependent ser/thr Calcineurin and has been used to describe the immunosuppressive action of cyclosporine. Cyclophilin can stabilize the cis-trans conformation transition state and speed up isomerization steps in protein folding. This process is important in the assembly of multiple domain proteins. Their existence as foldases and molecular chaperones enable them to be able to assist in the covalent folding or unfolding and the assembly or disassembly of other macromolecular structures.

EGFR as a Negative Regulatory Protein Adjusts the Activity and Mobility of NHE3 in the Cell Membrane of IPEC-J2 Cells With TGEV Infection.

Transmissible gastroenteritis (TGE) has caused devastating economic losses to the swine industry worldwide, despite extensive research focusing on the pathogenesis of virus infection. The molecular pathogenic mechanism of TGEV-induced diarrhea in piglets is unknown. Intestinal diarrhea is closely related to the function of the Na+/H+ exchanger protein NHE3 in the brush border membrane of small intestine epithelial cells. The epidermal growth factor receptor (EGFR) may act to regulate NHE3 expression. In addition, EGFR may promote viral invasion of host cells. The present study aimed to determine whether NHE3 activity is regulated by altering EGFR expression to affect Na+ absorption in TGEV-infected intestinal epithelial cells. Porcine intestinal epithelial cells were used as models for TGEV infection. The results showed that Na+ absorption and NHE3 expression levels decreased in TGEV-infected cells. Proliferation of TGEV within IPEC-J2 cells could be inhibited by treatment with the EGFR inhibitor AG1478 and knockdown; resulting in recovery of Na+ absorption in TGEV infected cells and increasing the activity and expression of NHE3. Moreover, we demonstrated that NHE3 activity was regulated through the EGFR/ERK pathway. Importantly, NHE3 mobility on the plasma membrane of TGEV infected cells was significantly weaker than that in normal cells, and EGFR inhibition and knockdown recovered this mobility. Our research indicated that NHE3 activity was negatively regulated by EGFR in TGEV-infected intestinal epithelial cells.

Characterization of Critical Functions of Long Non-Coding RNAs and mRNAs in Rhabdomyosarcoma Cells and Mouse Skeletal Muscle Infected by Enterovirus 71 Using RNA-Seq.

Enterovirus 71 (EV71) is the main pathogen of severe hand-foot-mouth disease (HFMD). Long non-coding RNAs (lncRNAs) are recognized as pivotal factors during the pathogenesis of viral infection. However, the critical functions of lncRNAs in EV71–host interactions have not been characterized. Here, for the first time, we performed global transcriptome analysis of lncRNA and mRNA expression profiles in EV71-infected human rhabdomyosarcoma (RD) cells and skeletal muscle of mice using second-generation sequencing. In our study, a total of 3801 novel lncRNAs were identified. In addition, 23 lncRNAs and 372 mRNAs exhibited remarkable differences in expression levels between infected and uninfected RD cells, while 104 lncRNAs and 2647 mRNAs were differentially expressed in infected skeletal muscle from neonatal mice. Comprehensive bioinformatics analysis included target gene prediction, lncRNA-mRNA co-expression network construction, as well as gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis mainly focused on differentially-expressed genes (DEGs). Our results suggest that lncRNAs may participate in EV71 infection-induced pathogenesis through regulating immune responses, protein binding, cellular component biogenesis and metabolism. The present study provides novel insights into the functions of lncRNAs and the possible pathogenic mechanism following EV71 infection.

Exosome Biogenesis and Biological Function in Response to Viral Infections.

Introduction:Exosomes are extracellular vesicles that originate as intraluminal vesicles during the process of multivescular body formation. Exosomes mediate intercellular transfer of functional proteins, lipids, and RNAs. The investigation into the formation and role of exosomes in viral infections is still being elucidated. Exosomes and several viruses share similar structural and molecular characteristics.Explanation:It has been documented that viral hijacking exploits the exosomal pathway and mimics cellular protein trafficking. Exosomes released from virus-infected cells contain a variety of viral and host cellular factors that are able to modify recipient host cell responses. Recent studies have demonstrated that exosomes are crucial components in the pathogenesis of virus infection. Exosomes also allow the host to produce effective immunity against pathogens by activating antiviral mechanisms and transporting antiviral factors between adjacent cells.Conclusion:Given the ever-growing roles and importance of exosomes in both host and pathogen response, this review will address the impact role of exosome biogenesis and composition after DNA, RNA virus, on Retrovirus infections. This review also will also address how exosomes can be used as therapeutic agents as well as a vaccine vehicles.

Radiographic and CT Features of Viral Pneumonia.

Viruses are the most common causes of respiratory infection. The imaging findings of viral pneumonia are diverse and overlap with those of other nonviral infectious and inflammatory conditions. However, identification of the underlying viral pathogens may not always be easy. There are a number of indicators for identifying viral pathogens on the basis of imaging patterns, which are associated with the pathogenesis of viral infections. Viruses in the same viral family share a similar pathogenesis of pneumonia, and the imaging patterns have distinguishable characteristics. Although not all cases manifest with typical patterns, most typical imaging patterns of viral pneumonia can be classified according to viral families. Although a definite diagnosis cannot be achieved on the basis of imaging features alone, recognition of viral pneumonia patterns may aid in differentiating viral pathogens, thus reducing the use of antibiotics. Recently, new viruses associated with recent outbreaks including human metapneumovirus, severe acute respiratory syndrome coronavirus, and Middle East respiratory syndrome coronavirus have been discovered. The imaging findings of these emerging pathogens have been described in a few recent studies. This review focuses on the radiographic and computed tomographic patterns of viral pneumonia caused by different pathogens, including new pathogens. Clinical characteristics that could affect imaging, such as patient age and immune status, seasonal variation and community outbreaks, and pathogenesis, are also discussed. The first goal of this review is to indicate that there are imaging features that should raise the possibility of viral infections. Second, to help radiologists differentiate viral infections, viruses in the same viridae that have similar pathogenesis and can have similar imaging characteristics are shown. By considering both the clinical and radiologic characteristics, radiologists can suggest the diagnosis of viral pneumonia. ©RSNA, 2018.