2016 International meeting of the Global Virus Network

The Global Virus Network (GVN) was established in 2011 in order to strengthen research and responses to current viral causes of human disease and to prepare against new viral pandemic threats. There are now 38 GVN Centers of Excellence and 6 Affiliate laboratories in 24 countries. GVN scientists meet annually to learn about each other's current research, address collaborative priorities and plan future programs. The 2016 meeting was held from October 23e25 in Hokkaido, Japan, in partnership with the Japanese Society for Virology, the National Institute of Infectious Diseases of Japan and the Research Center for Zoonosis Control of Hokkaido University. This report highlights the accomplishments of GVN researchers in many priority areas of medical virology, including the current Zika epidemic, infections by human papillomavirus, influenza, Ebola, Lassa, dengue, HIV, hepatitis C, and chikungunya viruses, and the development of improved diagnostics and new vaccines.Instituto de Biotecnologia y Biologia Molecula

2016 International meeting of the Global Virus Network

The Global Virus Network (GVN) was established in 2011 in order to strengthen research and responses to current viral causes of human disease and to prepare against new viral pandemic threats. There are now 38 GVN Centers of Excellence and 6 Affiliate laboratories in 24 countries. GVN scientists meet annually to learn about each other's current research, address collaborative priorities and plan future programs. The 2016 meeting was held from October 23e25 in Hokkaido, Japan, in partnership with the Japanese Society for Virology, the National Institute of Infectious Diseases of Japan and the Research Center for Zoonosis Control of Hokkaido University. This report highlights the accomplishments of GVN researchers in many priority areas of medical virology, including the current Zika epidemic, infections by human papillomavirus, influenza, Ebola, Lassa, dengue, HIV, hepatitis C, and chikungunya viruses, and the development of improved diagnostics and new vaccines.Instituto de Biotecnologia y Biologia Molecula

Effect of genetic background and delivery route on the preclinical properties of a live attenuated RSV vaccine.

A safe and effective vaccine against RSV remains an important unmet public health need. Intranasally (IN) delivered live-attenuated vaccines represent the most extensively studied approach for immunization of RSV-naïve infants and children, however, achieving an effective balance of attenuation and immunogenicity has proven challenging. Here we report pre-clinical immunogenicity and efficacy data utilizing a live-attenuated vaccine candidate, RGΔM2-2, which was obtained by deleting the M2-2 open reading frame from the genome of the MSA1 clinical isolate. Intramuscular (IM) administration of RGΔM2-2 in cotton rats induced immunity and protective efficacy that was comparable to that induced by intranasal (IN) immunization. In contrast, the protective efficacy of RGΔM2-2 delivered by the IM route to African green monkeys was substantially reduced as compared to the efficacy following IN administration, despite comparable levels of serum neutralizing antibodies. This result suggests that mucosal immunity may play an important role in RSV protection. The RGΔM2-2 vaccine also demonstrated different attenuation profiles when tested in cotton rats, non-human primates, and a human airway epithelial (HAE) cell model. The data suggest RGΔM2-2 is less attenuated than a similarly designed vaccine candidate constructed on the A2 genetic background. These findings have important implications with regard to both the design and the preclinical safety testing of live-attenuated vaccines

Growth of RGΔM2-2 versus parental virus in Vero cells.

<p>(A) Vero cells were infected at an MOI of 0.001 and incubated at 37°C. Samples harvested at the times indicated were titrated on Vero cells.</p

Attenuation and immunogenicity in cotton rats.

<p>(A) Groups of cotton rats were infected as indicated. (B) The degree of attenuation as amount of virus present in the lungs of animals in (A) was determined. ****p < 0.0001 by unpaired t test. (C) Immunogenicity study in cotton rats. Animals were immunized as indicated. (D) Serum neutralization titers were determined. (E) Protective efficacy as amount of challenge virus present in the lungs of immunized animals in (C).</p

IN vs IM immunization in NHP.

<p>(A) AGMs were infected as indicated. (B) Serum F-binding antibodies were determined by ELISA. (C) Complement-dependent serum neutralizing titers were measure by PRNT60. (D) Protective efficacy determined as virus titers from BAL samples after challenge.</p

IM boost immunization in NHP.

<p>(A) AGMs were infected as indicated. (B) Complement-dependent serum neutralizing titers, PRNT60. (C) Protective efficacy as determined from BAL samples after challenge.</p