Effect Of Virus Infection Research Articles

Extracellular DNA can preserve the genetic signatures of present and past viral infection events in deep hypersaline anoxic basins

Deep hypersaline anoxic basins (DHABs) of the Mediterranean Sea are among the most extreme ecosystems on Earth and host abundant, active and diversified prokaryotic assemblages. However, factors influencing biodiversity and ecosystem functioning are still largely unknown. We investigated, for the first time, the impact of viruses on the prokaryotic assemblages and dynamics of extracellular DNA pool in the sediments of La Medee, the largest DHAB found on Earth. We also compared, in La Medee and L'Atalante sediments, the diversity of prokaryotic 16S rDNA sequences contained in the extracellular DNA released by virus-induced prokaryotic mortality. We found that DHAB sediments are hot-spots of viral infections, which largely contribute to the release of high amounts of extracellular DNA. DNase activities in DHAB sediments were much higher than other extracellular enzymatic activities, suggesting that extracellular DNA released from killed prokaryotes can be the most suitable trophic resource for benthic prokaryotes. Preserved extracellular DNA pools, which contained novel and diversified gene sequences, were very similar between the DHABs but dissimilar from the respective microbial DNA pools. We conclude that the strong viral impact in DHAB sediments influences the genetic composition of extracellular DNA, which can preserve the signatures of present and past infections.

Lactate dehydrogenase-elevating virus infection: an experimental model of immune microenvironment modulation.

Lactate dehydrogenase-elevating virus (LDV), a mouse arterivirus, is characterized by a lifelong viremia, despite antiviral innate and adaptative immune response. It induces strong modifications of the host immune microenvironment, including macrophage and natural killer cell activation, secretion of pro-inflammatory cytokines, modulation of T helper cell differentiation and polyclonal activation of B-lymphocytes. This modification of the immune microenvironment results in the protection against some diseases such as allergies, graft-versus-host reaction, experimental autoimmune encephalitis, and growth of some tumors. In contrast, it exacerbates other pathologies such as endotoxin shock and autoantibody-mediated autoimmune diseases. Thus, LDV infection provides an interesting model to understand the consequences of viral infections on pathogenic mechanisms and to define new therapeutic approaches.

Viruses Induce Type 1 Diabetes Mellitus in the Presence of HLA-DR3, DR4 Genes

Recently, the increasing of type 1 diabetes (T1DM) was revealed among children in Kurdistan - Iraq that passed through several wars and economic sanctions. It has been demonstrated that virus infection induced T1DM by destruction of beta cells through direct invasion or autoimmune reactions. Genetic factors also lead to immune disorders which induce T1DM. Despite the reports on effects of viral infection and autoimmune disturbance in the presence of HLA genes, there are no enough studies to show the relationship between them in Kurdish race. Therefore, Serum glucose, three viral (CMV, Rubella and Coxsackie virus), two genes (HLA DR3 and HLA DR4) and anti- glutamic acid decarboxylase (GAD) Ab. were studied to evaluate their relationship with T1DM. Study was performed by interviewing 230 samples (122 females and 108 males) of T1DM patients and another 130 non-diabetic individuals as a control group for collecting blood samples and personal and family information related to this study. Indirect Enzyme-Linked Immuno Sorbent Assay (ELISA) used for detection of anti-viruses antibodies and anti-GAD antibody. While, Polymerase Chain Reaction (PCR) - SSP technique were used for detection of HLA-DR3 and DR4. The statistical results revealed that the mean±SD concentration of anti-CMV IgG, rubella, CSV-B antibodies in the sera of patients was (1.22±0.36 IU/ml), (0.80±0.08 IU/ml), (0.81±0.14 IU/ml) respectively when compared with (0.79±0.32 IU/ml), (0.38±0.17 IU/ml), (0.26±0.21 IU/ml) respectively in sera of control group (P-value < 0.05). This means that there is a significant increase in mean concentration of anti-CMV, rubella, CSV-B antibodies in the sera of patients in comparison with control group. The mean of anti-GAD antibody was (89.54±0.43 IU/ml) when compared with (9.73±38 IU/ml) with control group (P-value < 0.05). While, results of the HLA-DR3 and DR4 genes revealed that there are a relationship between these genes and viral infections that induce T1DM and these genes also related with the elevation of anti-GAD Ab in the blood circulation of T1DM patients. This study supports the claims that viruses are responsible for T1DM especially in the presence of HLA-DR3 or/and DR4.

Elevated risk of opportunistic viral infection in patients with Crohn’s disease during biological therapies: a meta analysis of randomized controlled trials

Biological agents have been widely used in the treatment of Crohn's disease (CD). These drugs carry the risk of excessive immunosuppression, indicating possible opportunistic infections including opportunistic viral infections, but no meta analysis has ever focused on this issue. To evaluate whether there is an association between biological agents therapy and the risk of opportunistic viral infections and serious infections in patients with CD. A search of online databases was performed and literature selection was carried out according to the inclusion and exclusion criteria by reading titles, abstracts and full texts. Study heterogeneity and publication bias were assessed. Whether to choose a fixed effects model or a random effects model depended on the result of heterogeneity test. There was a statistical significance in opportunistic viral infection events between the biological agents group and the placebo group. However, our analysis didn't observe statistically significant differences between the two groups when combined analyses were carried out for herpes zoster and herpes simplex separately. A risk trend in the biological agents group was observed in the analysis for herpes zoster. More analyses aimed at the outcome measures and including influenza and serious infection were carried out separately, but no statistical significance was found in them. Biological agents use might increase the risk of opportunistic viral infections in patients with CD, but not the risk of herpes simplex and serious infections. More randomized controlled trials (RCTs) are needed to draw the conclusion of whether they could elevate the risk of herpes zoster.

Adoptive T-cell therapy to treat liver cancer: Is the liver microenvironment key?

Hepatocellular carcinoma (HCC) reflects the 5th most common cause for cancer related deaths worldwide with approximately 800.000 deceases per year and is the third most frequent cause for death worldwide [1]. In African or Asian countries HCC has become the most common cause for cancer-related death, mainly as a consequence of viral infections with Hepatitis B and C-viruses (HBV; HCV). Notably, in Europe and the USA HCC is on the rise, reflecting the fastest increasing cancer type in recent years in the USA. Prospectively this trend will worsen in the USA and Europe since e.g. HCV had already superseded HIV as a cause of death. Moreover, in industrialized countries not only HBV- or HCV-infections surmount this development but more and more high fat diet induced non-alcoholic steatohepatitis (NASH) and non-alcoholic fatty liver disease (NAFLD) lead to liver cancer [1]. Given the effort that has been invested in the past year to understand and treat HCC - either induced by viruses, high fat diet or chronic alcohol consumption - clinical success has been relatively small. Up to now the most effective intervention to prolong life-span of HCC patients has been liver transplantation for those with a single, small nodule – which is the exception. Chemo- and radiotherapy do not lead to an amelioration of the patient's status but rather to tumor cell resistance in patients with HCC. Moreover, the aberrant liver function of HCC patients rather reduces the efficacy of the chemotherapy than promoting it. Various novel drugs have been investigated, and the pantyrosine kinase inhibitor Sorafenib [1] has become the standard of care for HCC therapy. Except transplantation, these regimens, however, are rather palliative than curative [1]. Thus, apart from the demand to broaden HCC surveillance programs to reduce overall disease specific mortality for people at risk, an efficient therapy to treat HCC is urgently needed. In contrast to the antigenic heterogeneity of high fat diet or alcohol induced HCC, that express tumor-associated (self) antigens or individually mutated antigens, tumor cells of virus-induced HCC equally express - and may be addicted to - viral proteins, that are recognized by the immune system. Nevertheless, virus-induced HCC often escapes immune-surveillance. In a related virus-induced HCC mouse model we have shown that tumor-specific T cells are functionally activated by the virus infection but that the developing HCC escapes destruction since T cells can only poorly infiltrate HCC and the few remaining, infiltrating T cells are rendered dysfunctional in the liver [2]. Therefore, immunotherapy for treating virus-induced HCC, in particular adoptively transferred T-cells targeted against viral oncogenes acting as shared tumor-specific antigens, could represent a very promising and successful approach.

Acquisition of Contextual Discrimination Involves the Appearance of a RAS-GRF1/p38 Mitogen-activated Protein (MAP) Kinase-mediated Signaling Pathway That Promotes Long Term Potentiation (LTP)

RAS-GRF1 is a guanine nucleotide exchange factor with the ability to activate RAS and RAC GTPases in response to elevated calcium levels. We previously showed that beginning at 1 month of age, RAS-GRF1 mediates NMDA-type glutamate receptor (NMDAR)-induction of long term depression in the CA1 region of the hippocampus of mice. Here we show that beginning at 2 months of age, when mice first acquire the ability to discriminate between closely related contexts, RAS-GRF1 begins to contribute to the induction of long term potentiation (LTP) in the CA1 hippocampus by mediating the action of calcium-permeable, AMPA-type glutamate receptors (CP-AMPARs). Surprisingly, LTP induction by CP-AMPARs through RAS-GRF1 occurs via activation of p38 MAP kinase rather than ERK MAP kinase, which has more frequently been linked to LTP. Moreover, contextual discrimination is blocked by knockdown of Ras-Grf1 expression specifically in the CA1 hippocampus, infusion of a p38 MAP kinase inhibitor into the CA1 hippocampus, or the injection of an inhibitor of CP-AMPARs. These findings implicate the CA1 hippocampus in the developmentally dependent capacity to distinguish closely related contexts through the appearance of a novel LTP-supporting signaling pathway.

Increase in Gut Microbiota after Immune Suppression in Baculovirus-infected Larvae

Spodoptera exigua microarray was used to determine genes differentially expressed in S. exigua cells challenged with the species-specific baculovirus SeMNPV as well as with a generalist baculovirus, AcMNPV. Microarray results revealed that, in contrast to the host transcriptional shut-off that is expected during baculovirus infection, S. exigua cells showed a balanced number of up- and down-regulated genes during the first 36 hours following the infection. Many immune-related genes, including pattern recognition proteins, genes involved in signalling and immune pathways as well as immune effectors and genes coding for proteins involved in the melanization cascade were found to be down-regulated after baculovirus infection. The down-regulation of immune-related genes was confirmed in the larval gut. The expression of immune-related genes in the gut is known to affect the status of gut microorganisms, many of which are responsible for growth and development functions. We therefore asked whether the down-regulation that occurs after baculovirus infection affects the amount of gut microbiota. An increase in the gut bacterial load was observed and we hypothesize this to be as a consequence of viral infection. Subsequent experiments on virus performance in the presence and absence of gut microbiota revealed that gut bacteria enhanced baculovirus virulence, pathogenicity and dispersion. We discuss the host immune response processes and pathways affected by baculoviruses, as well as the role of gut microbiota in viral infection.

Interaction of Cucumber mosaic virus and Bean yellow mosaic virus in co-infected plants of bean and broad bean

After evaluation of the responses of bean and broad bean common cultivars against an isolate of Cucumber mosaic virus (CMV-K) and Bean yellow mosaic virus (BYMV-K), interaction of isolates was statistically studied on co-infected plants of bean cv. Bountiful and broad bean cv. Lahijan at two trials. Based on viral relative concentration determined by quantitative enzyme-linked immunosorbent assay, BYMV interacts synergistically with CMV in bean at 14 days post inoculation, while in co-infection with BYMV, CMV interacts antagonistically in both host plants at least in one of the two trials. This suggests that CMV/BYMV interaction is dependent on host species and developmental stage of plant. Co-infection like single infection with CMV in bean plants led to significantly decrease in plants’ height and fresh weight than BYMV singly infected and healthy plants, while viral infection of broad bean plants did not significantly affect growth parameters. Decline effect of viral infection (especially co-infection) on chlorophyll and carotenoids value of bean plants was greater than those of broad bean. Viral infection (singly or doubly) caused irregular changes in nutrient elements values of both hosts compared with healthy ones.

メロン黄化えそウイルスの感染が黄化えそ病中程度抵抗性を有するキュウリ安濃4号および罹病性品種の生育と収量に及ぼす影響

メロン黄化えそウイルス（MYSV）の感染が黄化えそ病に中程度の抵抗性を有するキュウリ安濃4号および罹病性品種の生育と収量性に及ぼす影響を調べた．キュウリ安濃4号では，MYSVに感染しても植物体の生育は，罹病性品種に比べそれほど抑制されなかったが，罹病性品種では，葉は小さく，側枝の伸張は大きく抑制された．ウイルス接種区におけるキュウリ安濃4号の収量は，対無接種区比で79～88％になり，モザイク果は認められなかった．一方，罹病性品種の収量は，対無接種区比で32～52％で，モザイク果の発生が認められた．キュウリ安濃4号は，MYSVに感染しても収量の低下が1～2割程度に抑制可能であり，本系統が有する中程度抵抗性は実用的に利用可能であると考えられた．

Viruses as triggers of DNA rearrangements in host plants

Andronic, L. 2012. Viruses as triggers of DNA rearrangements in host plants. Can. J. Plant Sci. 92: 1083-1091. Assessment of microsporogenesis in tomato (Lycopersicon esculentum, cultivars Fachel, Nistru and Prizior) infected with tomato aspermy virus or potato virus X and barley (Hordeum vulgare L., cultivars Galactic, Sonor, Unirea) infected with barley stripe mosaic virus showed deviations in the conjugation of homologous chromosomes and segregation of genetic material, expressed in the disruption of chromatin cohesion between homologous chromosomes. The evidence of meiotic division in targeted genotypes indicates the effect of viral infection on chiasmata number and position, promoting the redistribution of chiasmata. On the basis of cytological study, significant changes and the induction of additional exchanges offset by asynapsis were established in early diakinesis. Different parameters, determined at particular stages of meiosis, such as chromosome aberration and the mean percentage of abnormal p...

Viruses as triggers of DNA rearrangements in host plants

Andronic, L. 2012. Viruses as triggers of DNA rearrangements in host plants. Can. J. Plant Sci. 92: 1083–1091. Assessment of microsporogenesis in tomato (Lycopersicon esculentum, cultivars Fachel, Nistru and Prizior) infected with tomato aspermy virus or potato virus X and barley (Hordeum vulgare L., cultivars Galactic, Sonor, Unirea) infected with barley stripe mosaic virus showed deviations in the conjugation of homologous chromosomes and segregation of genetic material, expressed in the disruption of chromatin cohesion between homologous chromosomes. The evidence of meiotic division in targeted genotypes indicates the effect of viral infection on chiasmata number and position, promoting the redistribution of chiasmata. On the basis of cytological study, significant changes and the induction of additional exchanges offset by asynapsis were established in early diakinesis. Different parameters, determined at particular stages of meiosis, such as chromosome aberration and the mean percentage of abnormal pollen mother cells, served as cytogenetic evaluation of microsporogenesis in virus-infected tomato or barley cultivars. The study of meiotic stability in anaphase and telophase I and II revealed a significant increase in different types of abnormalities: elimination or/and lagging chromosomes, formation of chromosome and chromatid bridges with or without fragments. Reviewed examples provide data regarding genetic rearrangements in host plants as a response to viral infection.

DHEA inhibits Measles Virus through a Mechanism Independent of its ability to Modulate the Raf/MEK/ERK Signaling Pathway

Aim: Despite the existence of an effective vaccine, measles infection is still frequent in many developing countries with reduced health infrastructure, and it is one of the major causes of child death globally. In the past decade numerous outbreaks have occurred in developed countries, giving a fresh impetus to antiviral research against measles virus. The aim of this study was to investigate the antiviral activity of the natural steroid hormone DHEA against measles virus and the role of the Raf/MEK/ERK signaling pathway in viral multiplication and DHEA’s antiviral activity. Materials &amp; methods: The antiviral activity of DHEA and two ERK modulators, UO126 and anisomycin, was determined using a virus yield reduction assay. Furthermore, we studied DHEA’s virucidal activity and the viral multiplication step affected by the compound. The effect of virus infection on the Raf/MEK/ERK pathway and the activity of those compounds against measles virus spread and induced cytopathic effect were studied using western blot and indirect immunofluorescence. Results &amp; conclusion: We found that DHEA and UO126 are active against measles virus and that they are able to diminish virus-induced cytopathic effects. Also, our study showed that early events in the viral multiplication cycle trigger ERK activation, suggesting that DHEA, a Raf/MEK/ERK modulator, may not exert its antiviral activity through the modulation of this pathway. Our results may provide a first step in the development of new antiviral agents against measles virus.

Viral infections: A tale of two genomes

Approximately 200 viruses cause human diseases, from common colds to certain cancers. Viruses cannot replicate outside their host's cells; instead, they subvert the patients' cellular machinery to create new viral particles. While researchers and clinicians, including nurses, have made considerable progress in tackling viral infections, a combination of rapid replication and errors copying the virus's genetic code often produces mutations that are resistant to initially promising vaccines and antivirals. However, recent studies that decipher the viral genome help clinicians optimize treatment efficacy, trace the spread of diseases, and explain why new pandemics emerge. Viruses and their hosts have co-evolved for millions of years, and humans developed several lines of antiviral defences—and these lines continue to evolve as, for example, viruses change to overcome modern treatments. Studies into the interactions between viruses and their host cells helps explain, for example, why some people do not contract HIV despite being at high risk for many years. Scientists also identified numerous variations (polymorphisms) in the genes encoding human antiviral defences that help determine clinical and therapeutic outcomes. Understanding the genetics and lifecycle of viruses helps nurses understand the clinical consequences of viral infections, suggest or prescribe the most effective approaches to management, and identify opportunities to augment infection control. As this feature illustrates, the risk of infection, the severity of the resulting disease, and the effectiveness of treatment may depend on the interplay between two genomes.

P126 Defective type I IFNS production by plasmacytoid dendritic cells impairs T cell responses and virus control in early life

Introduction Cytopathic viruses causing acute infections in immunologically mature hosts often follow a prolonged course in early life, characterized by high viral titers maintained for several weeks. Accordingly, lymphocytic choriomeningitis virus (LCMV, WE strain) runs an acute course in adults but a protracted course in infant BALB/c mice, in which LCMV-specific CD8 + and CD4 + T cells fail to expand and control infection. To identify whether these defects were due to a dysfunction of innate immunity in infant mice, we analyzed early events of viral infection. Methods Type I IFN production was assessed early after LCMV infection of infant (2-week-old) and adult mice by ELISA and real-time PCR. We compared viral titers (by plaque assay) and T cell responses (by FACS) of LCMV-infected infant/adult wild-type and infant/adult IFNAR −/− mice. Activation and function of plasmacytoid and conventional dendritic cells were analyzed by FACS and real-time PCR. The effect of supplementing recombinant IFN-alpha early after infection on viral control and T cell responses was investigated in infant mice. Results Our data showed an insufficient immediate-early IFN-alpha production in infant mice, which fails to support early viral control and the expansion of LCMV-specific T cells: disrupting IFNAR signaling in adult mice mimicked a protracted LCMV infection. Plasmacytoid dendritic cells (pDCs) which are the main source of type I IFNs in LCMV infection failed to acquire an activated phenotype in infant mice and displayed defective function in vivo upon LCMV infection reflected by the low expression of the central pDC transcription factor E2-2 and related genes (TLR7/9, IRF-7 and IRF-8), MyD88 and NF-KappaB. In contrast, the in vitro function of early life pDCs was normal suggesting an in vivo negative regulation of infant pDCs. Direct evidence of the contribution of type I IFNs for early life infection control was demonstrated by given exogenous IFN-alpha which restored virus control and CTL functionality in infant mice. Conclusion In this study, we identify an age-specific down-regulation of multiple factors which are critical for the activation and function of pDCs and demonstrate that it is orchestrated by the E2-2 pDC regulator. We show that this down-regulation prevents the immediate-early burst of type I IFN and the early viral control and permanently impairs CD4 + and CD8 + T cell responses. The results suggest that early life pDC responses are tightly regulated in vivo , possibly to avoid potentially harmful inflammatory or autoimmune reactions. This concept offers novel opportunities for prevention and therapy of infectious complications in early life.

Loss of stress response as a consequence of viral infection: implications for disease and therapy

Herein, we propose that viral infection can induce a deficient cell stress response and thereby impairs stress tolerance and makes tissues vulnerable to damage. Having a valid paradigm to address the pathological impacts of viral infections could lead to effective new therapies for diseases that have previously been unresponsive to intervention. Host response to viral infections can also lead to autoimmune diseases like type 1 diabetes. In the case of Newcastle disease virus, the effects of viral infection on heat shock proteins may be leveraged as a therapy for cancer. Finally, the search for a specific virus being responsible for a condition like chronic fatigue syndrome may not be worthwhile if the disease is simply a nonspecific response to viral infection.

Involvement of interaction between viral VP466 and host tropomyosin proteins in virus infection in shrimp

The accumulating evidence indicates that the viral structural proteins play critical roles in virus infection. However, the interaction between the viral structural protein and host cytoskeleton protein in virus infection remains to be addressed. In this study, the viral VP466 protein, one of the major structural proteins of shrimp white spot syndrome virus (WSSV), was characterized. The results showed that the suppression of VP466 gene expression led to the inhibition of WSSV infection in shrimp, indicating that the VP466 protein was required in virus invasion. It was found that the VP466 protein was interacted with the host cytoskeleton protein tropomyosin. As documented, the VP466–tropomyosin interaction facilitated the WSSV infection. Therefore our findings revealed a novel molecular mechanism in the virus invasion to its host, which would be helpful to better understand the molecular events in virus infection in invertebrate.

Ultrastructure of the salivary glands of non-infected and infected glands in Glossina pallidipes by the salivary glands hypertrophy virus

Light, scanning electron, and transmission electron microscopy analyses were conducted to examine the morphology and ultrastructure of the salivary glands of Glossina pallidipes. Three distinct regions, each with a characteristic composition and organization of tissues and cells, were identified: secretory, reabsorptive and proximal. When infected with the salivary gland hypertrophy (SGH) virus, glands showed a severe hypertrophy, accompanied by profound changes in their morphology and ultrastructure. In addition, the muscular fibers surrounding the secretory region of the glands were disrupted. The morphological alterations in the muscular tissue, caused by viral infection, could be an important aspect of the pathology and may shed light on the mode of action of the SGH virus. Results were discussed with regard to the potential effect of viral infection on normal salivation and on the ability of infected tsetse flies to transmit a trypanosome parasite.

Advances in HIV Microbicide Development

There is an urgent need control the spread of the global HIV pandemic. A microbicide, or topical drug applied to the mucosal environment to block transmission, is a promising HIV prevention strategy. The development of a safe and efficacious microbicide requires a thorough understanding of the mucosal environment and its role in HIV transmission. Knowledge of the key events in viral infection identifies points at which the virus might be most effectively targeted by a microbicide. The cervicovaginal and rectal mucosa play an important role in the innate defense against HIV, and microbicides must not interfere with these functions. In this review, we discuss the current research on HIV microbicide development.

A case of peripheral and eosphagatic hypereosinophilia and food wllergy after liver’s transplantation in adult

From one year of liver's transplantation and cyclosporin (CSA) maintenance treatment(100 mg a day), a 43 years old women presented with abdominal pain and diarrhea immediately after eating milk and egg. She underwent the transplantation after an acute liver toxicity caused by isoniazid during tuberculosis treatment. Increasing hyperosinophilia (40%) and eosinophilic oesophagitis (EE) presented with food allergy. Total IgE were low (45UI). Commercial skin prick test and prick by prick as specific IgEs detection (IMMUNOCAP) were positive for milk's proteins, egg, rice and wheat flour. Hypereosinophilia persisted inspite of an elimination diet for the culprit allergens while the clinical symptoms of food allergy improved. Other causes of hypereosinophilia were excluded. Interestingly only an inhaled fluticasone propionate treatment (FP,250 mcg bid) for three months was followed by an outstanding reduction of EE and hypereosinophilia (less than 1000/mm3 and <25%) without changing CSA dosage. Food allergy and hypereosinophilia has been increasingly reported in children in the setting of liver transplantation during tacrolimus treatment.On the contrast reports in adults are very rare expecially during CSA treatment. In our patient elimination diet wasn't followed by a reduction of hypereosinofilia as generally occurs in pediatric cases. Our patient didn't present any allergy before the transpantation.No information was available on donor's known allergy. Different meccanisms are supposed underlying the new onset of food allergy and hypereosinophilia in liver's transplantation: • An imbalance between Th1/Th2 cells or an increased enteric permeability. • Immune effects of viral infections associated with the immunosoppressive state. • Acquired food allergy and hypereosinophilia due to a transfer of hepatic hematopoietic stam cells or active IGE from the donor's liver. More studied are needed in a controlled setting to identify similar findings among liver transplants.Moreover in the pretransplant investigation should be inlcluded the allergic status both of the donor as the recipient.

Zebrafish anti-apoptotic gene Bcl-xL can prevent aquatic birnavirus-induced cell death in fish cells without affecting expression of viral proteins

The aquatic birnavirus induces mitochondria-mediated cell death in fish; however, the molecular mechanism remains unknown. In the present study, we demonstrated that aquatic birnavirus-induced mitochondria-mediated cell death is regulated by the anti-apoptotic Bcl-2 family member, zfBcl-xL, which is anti-apoptotic and enhances host cell viability. First, CHSE-214 cells carrying EGFP-zfBcl-xL fused genes were selected, established in culture, and used to examine the involvement of zfBcl-xL in host cell protection from the effects of viral infection. EGFP-zfBcl-xL was found to prevent infectious pancreatic necrosis virus (IPNV)-induced phosphatidylserine exposure up to 40% at 12 h and 24 h post-infection (p.i.), block IPNV-induced loss of mitochondrial membrane potential (Δ Ψm), and enhance host viability at the middle and late replication stages. In addition, zfBcl-xL overexpression prevented IPNV-induced caspase-9 activation up to 25% and 85% at the middle (12 h p.i.) and late (24 h p.i.) replication stages without affecting expression of viral proteins such as VP3 (as a viral death protein) protein. In the present study, we demonstrated that aquatic birnavirus-induced cell death is prevented by the anti-apoptotic Bcl-2 family member, zfBcl-xL, which enhances host cell viability through blockage of mitochondrial disruption and caspase-9 activation.