Comparative analysis of infection and apoptosis in response to CHIKV infection.

<p>Summary of percentage infection (A) and apoptosis induction (B) in cell lines infected with CHIKV ECSA E1:226 V (226 V), CHIKV ECSA E1: A226 (A226), Ross strain (ROSS) or mock infected (Mock).</p

Infection and apoptosis in response to CHIKV E1:226 V infection.

<p>Summary of percentage infection (A) and apoptosis induction (B) in cell lines infected with CHIKV ECSA E1: 226 V (226 V) or mock infected (Mock).</p

Chikungunya Virus Infection of Cell Lines: Analysis of the East, Central and South African Lineage

<div><p>Chikungunya virus (CHIKV) is a re-emerging mosquito borne alphavirus that has caused large scale epidemics in the countries around the Indian Ocean, as well as leading to autochthonous transmission in some European countries. The transmission of the disease has been driven by the emergence of an African lineage of CHIKV with enhanced transmission and dissemination in <em>Aedes</em> mosquito hosts. Two main genotypes of this lineage have been circulating, characterized by the presence of a substitution of a valine for an alanine at position 226 of the E1 protein. The outbreak, numbering in millions of cases in the infected areas, has been associated with increasing numbers of cases with non-classical presentation including encephalitis and meningitis. This study sought to compare the original Ross strain with two isolates from the recent outbreak of chikungunya fever in respect of infectivity and the induction of apoptosis in eight mammalian cell lines and two insect cell lines, in addition to generating a comprehensive virus production profile for one of the newer isolates. Results showed that in mammalian cells there were few differences in either tropism or pathogenicity as assessed by induction of apoptosis with the exception of Hela cells were the recent valine isolate showed less infectivity. The Aedes albopictus C6/36 cell line was however significantly more permissive for both of the more recent isolates than the Ross strain. The results suggest that the increased infectivity seen in insect cells derives from an evolution of the CHIKV genome not solely associated with the E1:226 substitution.</p> </div

Summary of susceptibility to infection and induction of apoptosis for three CHIKV isolates.

<p>0%≤⁃≤20%; 21%≤▴≤40%; 41%≤▴▴≤60%; 61%≤▴▴▴≤80%; 81%≤▴▴▴▴≤100%; <b>ND</b>: Not determined.</p

CHIKV infection of CHME-5 human microglial cells.

<p>A. CHME-5 cells were mock infected (M) or infected with CHIKV ECSA E1: 226 V (EV) at m.o.i. of 1. Infected cells and culture medium were collected daily and the medium assayed for levels of infectious CHIKV at the times indicated by standard plaque assay on Vero cells, while cells were assayed for infectivity and induction of apoptosis by flow cytometry after staining with an anti-alphavirus monoclonal antibody and FITC-conjugated Annexin V/propidium iodide respectively. B. CHME-5 cells were mock infected (M) or infected with ECSA CHIKV E1: A226 (EA), ECSA CHIKV E1: 226 V (EV) or Ross strain (RO) at m.o.i. of 1 and assayed for infectivity and induction of apoptosis by flow cytometry on the days indicated. All experiments were undertaken independently in triplicate with duplicate analysis of virus titers. Error bars show S.D. C to F. CHME-5 cells were mock infected (C) or infected with ECSA CHIKV E1: 226 V (D), ECSA CHIKV E1: A226 (E) or Ross strain (F) and on day 2 p.i. stained with a mouse anti-alphavirus monoclonal antibody followed by a FITC conjugated goat anti-mouse IgG polyclonal antibody (green). Nuclei of cells were stained with TO-PRO-3 iodide (red). Non-contrast adjusted merged images are shown.</p