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A chemokine gene expression signature derived from meta-analysis predicts the pathogenicity of viral respiratory infections
Stewart T Chang, Nicolas Tchitchek, Debashis Ghosh, Arndt Benecke, Michael G Katze
BMC Systems Biology , 2011, DOI: 10.1186/1752-0509-5-202
Abstract: From a compendium of 12 studies that included responses to influenza A subtype H5N1, reconstructed 1918 influenza A virus, and SARS coronavirus, we used meta-analysis to derive multiple gene expression signatures. We compared these signatures by their capacity to segregate biological conditions by pathogenicity and predict pathogenicity in a test data set. The highest-performing signature was expressed as a continuum in low-, medium-, and high-pathogenicity samples, suggesting a direct, analog relationship between expression and pathogenicity. This signature comprised 57 genes including a subnetwork of chemokines, implicating dysregulated cell recruitment in injury.Highly pathogenic viruses elicit expression of many of the same key genes as lower pathogenic viruses but to a higher degree. This increased degree of expression may result in the uncontrolled co-localization of inflammatory cell types and lead to irreversible host damage.The threat of a highly lethal viral pandemic remains large in the 21st century. In 2003 SARS-coronavirus (CoV) appeared in Asia and then spread globally, causing greater than 40% mortality in individuals over 60 years of age [1]. Since 1997 highly pathogenic avian influenza, influenza A subtype H5N1, has resulted in high mortality rates (between 33% and 100% depending on the population) [2]. Finally in 2009 swine-origin influenza virus A (SOIV) subtype H1N1 emerged in the Americas and led to a pandemic. As Neumann et al. have observed, this virus shares many characteristics with 1918 influenza which resulted in an estimated 50 million deaths [3]. Furthermore, as Ilyushina et al. have shown, SOIV may mutate into more pathogenic forms in as little as ten passages in cell culture [4].Injury to the host during respiratory viral infections such as influenza now appears to be the result of inappropriate host responses [5]. Deriving gene expression signatures of high pathogenicity that are robust to biological and experimental variation would b
Cannabinoids and Viral Infections  [PDF]
Carol Shoshkes Reiss
Pharmaceuticals , 2010, DOI: 10.3390/ph3061873
Abstract: Exogenous cannabinoids or receptor antagonists may influence many cellular and systemic host responses. The anti-inflammatory activity of cannabinoids may compromise host inflammatory responses to acute viral infections, but may be beneficial in persistent infections. In neurons, where innate antiviral/pro-resolution responses include the activation of NOS-1, inhibition of Ca 2+ activity by cannabinoids, increased viral replication and disease. This review examines the effect(s) of cannabinoids and their antagonists in viral infections.
Viral infections of the biliary tract  [cached]
Gupta Ekta,Chakravarti Anita
Saudi Journal of Gastroenterology , 2008,
Abstract: Bacterial infections of the biliary tract are often considered to be an important cause of acute cholangitis. Viral infections of the biliary tract however, are very often mistaken as viral hepatitis. This article highlights various viral causes of common biliary tract infections. Viral cholangitis is both less common and less discussed than viral hepatitis. Hepatotropic viruses (A, B, C, and E) are generally regarded as hepatocellular pathogens, yet cholangitic manifestations are now well described in association with these diseases. Systemic viral diseases also lead to cholangitis in varying proportion to hepatitis. Human immunodeficiency virus is associated with protean hepatic complications, including cholangitis due to several causes. Other systemic viruses, most notably those of the herpes virus family, also cause hepatic disease including cholangitis and possibly ductopenia in both immunocompromised and immunocompetent patients.
Dengue viral infections  [cached]
Gurugama Padmalal,Garg Pankaj,Perera Jennifer,Wijewickrama Ananda
Indian Journal of Dermatology , 2010,
Abstract: Dengue viral infections are one of the most important mosquito-borne diseases in the world. Presently dengue is endemic in 112 countries in the world. It has been estimated that almost 100 million cases of dengue fever and half a million cases of dengue hemorrhagic fever (DHF) occur worldwide. An increasing proportion of DHF is in children less than 15 years of age, especially in South East and South Asia. The unique structure of the dengue virus and the pathophysiologic responses of the host, different serotypes, and favorable conditions for vector breeding have led to the virulence and spread of the infections. The manifestations of dengue infections are protean from being asymptomatic to undifferentiated fever, severe dengue infections, and unusual complications. Early recognition and prompt initiation of appropriate supportive treatment are often delayed resulting in unnecessarily high morbidity and mortality. Attempts are underway for the development of a vaccine for preventing the burden of this neglected disease. This review outlines the epidemiology, clinical features, pathophysiologic mechanisms, management, and control of dengue infections.
Mast cells in viral infections
Piotr Witczak,Ewa Brzezińska-B?aszczyk
Post?py Higieny i Medycyny Do?wiadczalnej , 2012,
Abstract: There are some premises suggesting that mast cells are involved in the mechanisms of anti-virus defense and in viral disease pathomechanisms. Mast cells are particularly numerous at the portals of infections and thus may have immediate and easy contact with the external environment and invading pathogens. These cells express receptors responsible for recognition of virus-derived PAMP molecules, mainly Toll-like receptors (TLR3, TLR7/8 and TLR9), but also RIG-I-like and NOD-like molecules. Furthermore, mast cells generate various mediators, cytokines and chemokines which modulate the intensity of inflammation and regulate the course of innate and adaptive anti-viral immunity. Indirect evidence for the role of mast cells in viral infections is also provided by clinical observations and results of animal studies. Currently, more and more data indicate that mast cells can be infected by some viruses (dengue virus, adenoviruses, hantaviruses, cytomegaloviruses, reoviruses, HIV-1 virus). It is also demonstrated that mast cells can release pre formed mediators as well as synthesize de novo eicosanoids in response to stimulation by viruses. Several data indicate that virus-stimulated mast cells secrete cytokines and chemokines, including interferons as well as chemokines with a key role in NK and Tc lymphocyte influx. Moreover, some information indicates that mast cell stimulation via TLR3, TLR7/8 and TLR9 can affect their adhesion to extracellular matrix proteins and chemotaxis, and influence expression of some membrane molecules. Critical analysis of current data leads to the conclusion that it is not yet possible to make definitive statements about the role of mast cells in innate and acquired defense mechanisms developing in the course of viral infection and/or pathomechanisms of viral diseases.
Using gene expression profiles from peripheral blood to identify asymptomatic responses to acute respiratory viral infections
Alexander Statnikov, Nikita I Lytkin, Lauren McVoy, J?rn-Hendrik Weitkamp, Constantin F Aliferis
BMC Research Notes , 2010, DOI: 10.1186/1756-0500-3-264
Abstract: Using acute respiratory viral challenge microarray data, we developed a molecular signature that for the first time allowed for an accurate differentiation between uninfected subjects prior to viral inoculation and subjects who remained asymptomatic after the viral challenge.Our findings suggest that molecular signatures can be used to characterize immune responses to viruses and may improve our understanding of susceptibility to viral infection with possible implications for vaccine development.Acute respiratory viral infections cause significant morbidity and mortality in the United States and worldwide. Currently clinicians do not have practical means to make a timely and accurate diagnosis of acute viral respiratory infections and often resort to unnecessary antibiotic treatment, which increases healthcare costs and facilitates development of antibiotic resistance. Recently a novel approach was proposed for the diagnosis of acute respiratory infections based on microarray gene expression profiles from peripheral blood samples from human subjects [1]. Using human viral challenge studies with live human rhinovirus (HRV), respiratory syncytial virus (RSV), and influenza A, Zaas et al. developed an "acute respiratory viral response" 30-gene panviral signature that accurately identified symptomatic patients with viral infection. The same study also reported that gene expression profiles of subjects prior to viral inoculation (at baseline) were indistinguishable from profiles of subjects who received viral challenge but remained asymptomatic and uninfected. Given the high sensitivity of microarray technology, we were intrigued by the latter result and hypothesize that it was an artifact of data analysis. Since the gene expression dataset of Zaas et al. was deposited in the Gene Expression Omnibus, we were able to verify our hypothesis and discover significant differences between these two groups of samples. We demonstrate this by developing a molecular signature that
Macrolide Therapy in Respiratory Viral Infections
Jin-Young Min,Yong Ju Jang
Mediators of Inflammation , 2012, DOI: 10.1155/2012/649570
Abstract: Background. Macrolides have received considerable attention for their anti-inflammatory and immunomodulatory actions beyond the antibacterial effect. These two properties may ensure some efficacy in a wide spectrum of respiratory viral infections. We aimed to summarize the properties of macrolides and their efficacy in a range of respiratory viral infection. Methods. A search of electronic journal articles through PubMed was performed using combinations of the following keywords including macrolides and respiratory viral infection. Results. Both in vitro and in vivo studies have provided evidence of their efficacy in respiratory viral infections including rhinovirus (RV), respiratory syncytial virus (RSV), and influenza virus. Much data showed that macrolides reduced viral titers of RV ICAM-1, which is the receptor for RV, and RV infection-induced cytokines including IL-1β, IL-6, IL-8, and TNF-α. Macrolides also reduced the release of proinflammatory cytokines which were induced by RSV infection, viral titers, RNA of RSV replication, and the susceptibility to RSV infection partly through the reduced expression of activated RhoA which is an RSV receptor. Similar effects of macrolides on the influenza virus infection and augmentation of the IL-12 by macrolides which is essential in reducing virus yield were revealed. Conclusion. This paper provides an overview on the properties of macrolides and their efficacy in various respiratory diseases.
Nuclear Actin and Lamins in Viral Infections  [PDF]
Jakub Cibulka,Martin Fraiberk,Jitka Forstova
Viruses , 2012, DOI: 10.3390/v4030325
Abstract: Lamins are the best characterized cytoskeletal components of the cell nucleus that help to maintain the nuclear shape and participate in diverse nuclear processes including replication or transcription. Nuclear actin is now widely accepted to be another cytoskeletal protein present in the nucleus that fulfills important functions in the gene expression. Some viruses replicating in the nucleus evolved the ability to interact with and probably utilize nuclear actin for their replication, e.g., for the assembly and transport of capsids or mRNA export. On the other hand, lamins play a role in the propagation of other viruses since nuclear lamina may represent a barrier for virions entering or escaping the nucleus. This review will summarize the current knowledge about the roles of nuclear actin and lamins in viral infections.
Pregnancy and sexually transmitted viral infections  [cached]
Singhal P,Naswa S,Marfatia Y
Indian Journal of Sexually Transmitted Diseases , 2009,
Abstract: Viral infections in pregnancy are a major cause of morbidity and mortality for both mother and fetus. Viral STIs occur as surface infection and then gradually infect immunologically protected sites. Therefore, these are asymptomatic, hidden and hence underdiagnosed, persistent and difficult to treat. HSV, HPV, HBV, HIV and CMV (cytomegalovirus) are the common ones. Most of these are transmitted during intrapartum period. Proper screening, identification and treatment offered during prenatal period may help in preventing their complications. Twenty five percent of women with a history of genital herpes have an outbreak at some point during the last month of pregnancy. Acyclovir is the accepted efficacious and safe therapy for HSV in pregnancy. Globally, HPV infection is the most common sexually transmitted infection. Neonatal transmission can occur in the absence of clinically evident lesions. HPV 6 or 11 may lead to Juvenile Onset Recurrent Respiratory Papillomatosis (JORRP). TCA, liquid nitrogen, laser ablation or electrocautery can be used to treat external genital HPV lesions at any time during pregnancy. Cesarean section is recommended only if the lesions are obstructing the birth canal. Mother to child transmission (MTCT) in HIV accounts for 15-30% during pregnancy and delivery, and a further 5-20% of transmission occurs through breastfeeding. HBV infection during pregnancy does not alter the natural course of the disease. In women who are seropositive for both HBsAg and HBeAg, vertical transmission is approximately 90%. Pregnancy is not a contraindication for HBV vaccination. Cytomegalovirus (CMV) is the most common intrauterine infection. Cytomegalic inclusion disease (CID) is the most severe form of congenital CMV infection. Treatment is supportive.
Optimal Cytoplasmic Transport in Viral Infections  [PDF]
Maria R. D'Orsogna,Tom Chou
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0008165
Abstract: For many viruses, the ability to infect eukaryotic cells depends on their transport through the cytoplasm and across the nuclear membrane of the host cell. During this journey, viral contents are biochemically processed into complexes capable of both nuclear penetration and genomic integration. We develop a stochastic model of viral entry that incorporates all relevant aspects of transport, including convection along microtubules, biochemical conversion, degradation, and nuclear entry. Analysis of the nuclear infection probabilities in terms of the transport velocity, degradation, and biochemical conversion rates shows how certain values of key parameters can maximize the nuclear entry probability of the viral material. The existence of such “optimal” infection scenarios depends on the details of the biochemical conversion process and implies potentially counterintuitive effects in viral infection, suggesting new avenues for antiviral treatment. Such optimal parameter values provide a plausible transport-based explanation of the action of restriction factors and of experimentally observed optimal capsid stability. Finally, we propose a new interpretation of how genetic mutations unrelated to the mechanism of drug action may nonetheless confer novel types of overall drug resistance.
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