Showing papers by "Suresh Mahalingam published in 2007"
TL;DR: It is demonstrated that eosinophils can protect against RSV in vivo, as they promote virus clearance and may thus limit virus-induced lung dysfunction.
249 citations
TL;DR: It is demonstrated here that the complement system, an important component of the innate immune response, enhances the severity of RRV-induced disease in mice and suggested that complement plays an essential role in the effector phase, but not the inductive phase, of RRv-induced arthritis and myositis.
Abstract: Arthritogenic alphaviruses, including Ross River virus (RRV) and chikungunya virus, are mosquito-borne viruses that cause significant human disease worldwide, including explosive epidemics that can result in thousands to millions of infected individuals. Similar to infection of humans, infection of C57BL/6 mice with RRV results in severe monocytic inflammation of bone, joint, and skeletal muscle tissues. We demonstrate here that the complement system, an important component of the innate immune response, enhances the severity of RRV-induced disease in mice. Complement activation products were detected in the inflamed tissues and in the serum of RRV-infected wild-type mice. Furthermore, mice deficient in C3 (C3(-/-)), the central component of the complement system, developed much less severe disease signs than did wild-type mice. Complement-mediated chemotaxis is essential for many inflammatory arthritides; however, RRV-infected wild-type and C3(-/-) mice had similar numbers and composition of inflammatory infiltrates within hind limb skeletal muscle tissue. Despite similar inflammatory infiltrates, RRV-infected C3(-/-) mice exhibited far less severe destruction of skeletal muscle tissue. In addition to these studies, complement activation was also detected in synovial fluid from RRV-infected patients. Taken together, these findings indicate that complement activation occurs in the tissues of humans and mice infected with RRV and suggest that complement plays an essential role in the effector phase, but not the inductive phase, of RRV-induced arthritis and myositis.
102 citations
TL;DR: Alphaviruses were used to determine whether viruses grown in mosquito cells differed from mammalian-cell-derived viruses in their ability to induce type I interferon (IFN) responses in infected primary dendritic cells, and results suggest that the viruses initially delivered by the mosquito vector differ from those generated in subsequent rounds of replication in the host.
Abstract: Dendritic cells (DCs) are an important early target cell for many mosquito-borne viruses, and in many cases mosquito-cell-derived arboviruses more efficiently infect DCs than viruses derived from mammalian cells. However, whether mosquito-cell-derived viruses differ from mammalian-cell-derived viruses in their ability to induce antiviral responses in the infected dendritic cell has not been evaluated. In this report, alphaviruses, which are mosquito-borne viruses that cause diseases ranging from encephalitis to arthritis, were used to determine whether viruses grown in mosquito cells differed from mammalian-cell-derived viruses in their ability to induce type I interferon (IFN) responses in infected primary dendritic cells. Consistent with previous results, mosquito-cell-derived Ross River virus (mos-RRV) and Venezuelan equine encephalitis virus (mos-VEE) exhibited enhanced infection of primary myeloid dendritic cells (mDCs) compared to mammalian-cell-derived virus preparations. However, unlike the mammalian-cell-derived viruses, which induced high levels of type I IFN in the infected mDC cultures, mos-RRV and mos-VEE were poor IFN inducers. Furthermore, the poor IFN induction by mos-RRV contributed to the enhanced infection of mDCs by mos-RRV. These results suggest that the viruses initially delivered by the mosquito vector differ from those generated in subsequent rounds of replication in the host, not just with respect to their ability to infect dendritic cells but also in their ability to induce or inhibit antiviral type I IFN responses. This difference may have an important impact on the mosquito-borne virus's ability to successfully make the transition from the arthropod vector to the vertebrate host.
101 citations
TL;DR: This chapter summarizes the current understanding of viral arthritides using the newly developed mouse model of Ross River virus‐induced joint and muscle inflammation to summarized the mechanisms by which these viruses cause arthritis/arthralgia.
Abstract: Alphaviruses such as the Sindbis-group viruses, Scandinavian Ockelbo virus, the African Asian chikungunya virus, the African O'nyong-nyong virus, the South American Mayaro virus, and the Australasian Barmah Forest and Ross River viruses, are commonly associated with outbreaks of acute and persistent arthritis and arthralgia in humans. The mechanisms by which these viruses cause arthritis/arthralgia are poorly understood. This chapter summarizes our current understanding of viral arthritides using our newly developed mouse model of Ross River virus-induced joint and muscle inflammation.
73 citations
01 Jan 2007
TL;DR: Ross River virus is a mosquito transmitted disease endemic in tropical Australia, Papua New Guinea, East Timor, adjacent islands of Indonesia and the Solomon islands and it occurs epidemically in tempe.
Abstract: Ross River virus is a mosquito transmitted disease endemic in tropical Australia, Papua
New Guinea, East Timor, adjacent islands of Indonesia and the Solomon islands. It occurs
epidemically in tempe
8 citations