Robust Hepatitis C virus infection in vitro

Zhong J, Gastaminza P, Cheng GF, Kapadia S, Kato T, Burton DR, Wieland SF, Uprichard SL, Wakita T, Chisari FV. (2005). Robust Hepatitis C virus infection in vitro. PNAS 102 (26): 9294-9299.

Absence of a cell culture or animal model of hepatitis C virus (HCV) infection has limited analysis of the HCV life cycle. This also affects the development of effective antivirals and vaccines. In this study, the authors established a simple robust HCV cell culture infection system based on the JFH-1 molecular clone and HUH7 cell lines that allows production of the virus. Approximately 70% of HCV infected patients with acute infections progress to persistence, which often results in liver disease or cirrhosis. With >170 million people infected with HCV, this disease becomes a public health burden. This study bascially discusses how HCV is efficiently propagated in tissue culture.

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New Hope for Treatment of Painful Adult Shingles

http://www.sciencedaily.com/releases/2011/04/110421171718.htm
http://www.medicinenet.com/shingles/article.htm

Researchers at the University of Georgia and Yale University have discovered the treatment for shingles. Shingles is caused by the same virus that causes chickenpox and can be spread to people who have not had chickenpox and is also known as Herpes zoster. The rate of complications, including nerve pain can persist for months or years even after the shingles disappeared and it increases with age. shingles is becoming more prevalent, Researchers have discovered a novel and effective anti-shingles agent known as L-BHDA. Dr. Widener says that L-BHDA will allow patients to get well sooner and feel less pain, and will lessen their chances of complications

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Pulmonary surfactant prevents vaccinia infection

It has been recently discovered that lung surfactants are part of the body’s own innate immunity against viral infection!!! The primary function of pulmonary surfactants is to decrease the surface tension of water in the alveoli to prevent alveolar walls from sticking to each other. They are a phospholipoprotein with polar and non-polar regions and are secreted by type II cells found in the respiratory zone of the lungs.

In a study conducted by collaborators in France, researchers noticed interactions between the surfactant, Dipalmitoyl phosphatidylglycerol (DPPG), and vaccine virus (VACV). Vaccina is used as a surrogate to Variola virus which is the pathogen of smallpox. In order to study the interactions of DPPG and VACV, researchers used an in-vitro model of infection with human epithelial cell line A549. They performed various infection assays by which A549 cells were prophylactically treated with various types of surfactants including DPPG prior to infection by VACV. They discovered that DPPG significantly attenuated VACV infection. They also used electron microscopy to show that DPPG molecules physically attached to the VACV capsid which was believed to prevent infection by the virus.

Perino, J, Crouzier, D, & Spehner, D. (2011). Lung surfactant dppg phospholipid inhibits vaccinia virus infection. Antiviral Research, 89, 89-97.

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Hepatitis C Virus Infection in Phenotypically Distinct Huh7 Cell Lines

Sainz B, Barretto N, Uprichard SL. 2009. Hepatitis C Virus Infection in Phenotypically Distinct Huh7 Cell Lines.
PLoS 4(8):e6561. http://www.plosone.org/article/fetchSingleRepresentation.action?uri=info:doi/10.1371/journal.pone.0006561.s001

Over the years, scientists have been spending years trying to develop a model for HCV due to the lack of efficient viral infection model and culture systems. Until 2005, the first HCV infectious cell culture system was developed based on the Japanese FUlminant Hepatitis (JFH-1) molecular clone and human derived hepatoma cell line HUH7. HCV was isolated from patient from Japan with fulminant hepatitis. This patient was 32 years old and was admitted with symptoms of fatigue, high fever, and liver dysfunction. HCV RNA was detected by RT PCR and the patient was negative for antibodies to HCV. This JFH-1 strain replicates efficiently in HUH7 cells. This study basically outlines how this system is used and that this method will provide a powerful tool for studying the viral life cycle of HCV. The study of the HCV viral life cycle could leave opportunities for the construction of antivirals and effective vaccines.

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A Possible Norovirus Vaccine

This article discusses vaccines that are trying to be made in order to prevent norovirus infection. The norovirus causes diarrhea, vomiting, and stomach pain and is transmitted by fecal-oral contact or through contaminated food and water. It has been found that this virus is so contagious that only 10 viral particles are necessary in order to cause an infection. Therefore, scientists are trying to develop a vaccine against the norovirus. So, scientists inserted the human norovirus capsid gene into a different virus, which created a recombinant virus. Then, they used a vesicular stomatitis virus (VSV) which was used as a viral vector to deliver the recombinant virus and produce the virus like particles that mimic the actual human norovirus. This viral vector was effective in initiating an immune response and researchers were able to find that after two week of receiving the vaccine, the mice had developed and maintained high levels of antibodies against the human norovirus and developed a T cell immune response that was two times higher than the traditional vaccine group of mice. By using VSV as a vector, scientists were successful in creating an immune response in the mice and hope to use this as a future vaccine against the norovirus.

http://www.sciencedaily.com/releases/2011/03/110315130056.htm

http://www.cdc.gov/ncidod/dvrd/revb/gastro/norovirus.htm

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HIV Foils Our Efforts Again

A very promising new strategy for preventing the spread of HIV during unprotected sex sadly fell short.  The strategy was called pre-exposure prophylaxis, or PrEP for short, which consisted of an anti-HIV drug called Truvada.  The pill combined two antiretroviral drugs and was administered to individuals pre-infection with a high risk of contracting HIV.

In the original trial the drug was given to men and transgender women who have sex with men. The results of the first study were published in November of last year showing a 44% drop in HIV transmission compared to the placebo group.

In the second part of the study the drug was administered to heterosexual women.  Surprisingly the results of this study showed no differences compared to the placebo group.  The study conductors had several ideas for why this study fell short when the compared to the success of the first round but their main suspicion was that the women were not taking the drug as often as they should be based on discrepancies between self reports and blood analysis.  Further testing of blood samples can rule out participant error but the company producing the drug and running the trial has pulled the plug at least for now.

Here is a link to the original article published in November CLICK HERE

And a link to the recent article published this week CLICK HERE

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Impaired plasmacytoid dendritic cell maturation and differential chemotaxis in chronic hepatitis C virus: associations with antiviral treatment outcomes

Mengshol JA, Golden-Mason L, Castelblanco N, Im KA, Dillon SM, Wilson CC, and Rosen HR. (2009) Impaired plasmacytoid dendritic cell maturation and differential chemotaxis in chronic hepatitis C virus: associations with antiviral treatment outcomes. Gut 58:964-973.

Chronic hepatitis C (HCV) infection may be contributed to dendritic cell (DC) defects. DC are efficient antigen presenters and activators of antigen specific T cells and adaptive immunity. These cells may help determine the response of T cell stimulation to PEG-interferon and ribavirin therapy for HCV, but if the DC are defective, the claim was that there was a poor T cell response to HCV infection. In this study, matured DC defects and chemotaxis are used to compare therapeutic responders to non-responders. Samples of DC from 64 HCV-infected patients was analyzed 2 weeks before and 24 weeks after therapy. Flow cytometry was used to determine the amount of DCs and quantify chemokine receptor expression and an in vitro assay was used to measure chemotaxis. Results show that levels of CXCR3 and CXCR4 on DCs were higher compared to controls and decreased therapies. Pretreatment subjects of DCs were lower in HCV patients in comparison to the controls. Markers CD40 and CD83 were higher in DCs of patients infected with HCV compared to the controls. Chemotaxic of DCs to CXCL12 and CXCL10 showed failed antiviral responses. In conclusion, DC defects do occur in HCV patients, but successful antiviral therapy have normalized functional abnormalities.

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