Resurgence of chikungunya virus in India: an emerging threat

Saxena, Shailendra K.; Singh, Mugdha; Mishra, Niraj; Lakshmi, V

doi:10.2807/esw.11.32.03019-en

Cited by 35 publications

(29 citation statements)

References 5 publications

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“…Later, the virus was detected on the island of Réunion, where over 200 000 people were infected (Josseran et al, 2006). From Réunion, the virus spread to the Seychelles, Mauritius, Madagascar and finally India, with equally phenomenal numbers of infections (Ravi, 2006;Saxena et al, 2006). For example in India, it is estimated that over 1.3 million people across 13 states were infected (Arankalle et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Tracking epidemic Chikungunya virus into the Indian Ocean from East Africa

Njenga

Nderitu

Ledermann

et al. 2008

Journal of General Virology

165

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The largest documented outbreak of Chikungunya virus (CHIKV) disease occurred in the Indian Ocean islands and India during 2004–2007. The magnitude of this outbreak led to speculation that a new variant of the virus had emerged that was either more virulent or more easily transmitted by mosquito vectors. To study this assertion, it is important to know the origin of the virus and how the particular strain circulating during the outbreak is related to other known strains. This study genetically characterized isolates of CHIKV obtained from Mombasa and Lamu Island, Kenya, during 2004, as well as strains from the 2005 outbreak recorded in Comoros. The results of these analyses demonstrated that the virus responsible for the epidemic that spread through the Indian Ocean originated in coastal Kenya during 2004 and that the closest known ancestors are members of the Central/East African clade. Genetic elements that may be responsible for the scope of the outbreak were also identified.

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Section: Introductionmentioning

confidence: 99%

Tracking epidemic Chikungunya virus into the Indian Ocean from East Africa

Njenga

Nderitu

Ledermann

et al. 2008

Journal of General Virology

165

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“…Tanzania in 1953 (52, 69). The virus causes an acute febrile illness associated with severe joint pain that can persist long after viral clearance (9,26,42,47,49,62,68,75). In 2005 and 2006 CHIKV reemerged on a number of Indian Ocean islands and subsequently in India in 2006 and 2007 (78).…”

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confidence: 99%

Chikungunya Virus Induces IPS-1-Dependent Innate Immune Activation and Protein Kinase R-Independent Translational Shutoff

White

Sali

Alvarado

et al. 2011

J Virol

113

125

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Chikungunya virus (CHIKV) is an arthritogenic mosquito-transmitted alphavirus that is undergoing reemergence in areas around the Indian Ocean. Despite the current and potential danger posed by this virus, we know surprisingly little about the induction and evasion of CHIKV-associated antiviral immune responses. With this in mind we investigated innate immune reactions to CHIKV in human fibroblasts, a demonstrable in vivo target of virus replication and spread. We show that CHIKV infection leads to activation of the transcription factor interferon regulatory factor 3 (IRF3) and subsequent transcription of IRF3-dependent antiviral genes, including beta interferon (IFN-␤). IRF3 activation occurs by way of a virus-induced innate immune signaling pathway that includes the adaptor molecule interferon promoter stimulator 1 (IPS-1). Despite strong transcriptional upregulation of these genes, however, translation of the corresponding proteins is not observed. We further demonstrate that translation of cellular (but not viral) genes is blocked during infection and that although CHIKV is found to trigger inactivation of the translational molecule eukaryotic initiation factor subunit 2␣ by way of the double-stranded RNA sensor protein kinase R, this response is not required for the block to protein synthesis. Furthermore, overall diminution of cellular RNA synthesis is also observed in the presence of CHIKV and transcription of IRF3-dependent antiviral genes appears specifically blocked late in infection. We hypothesize that the observed absence of IFN-␤ and antiviral proteins during infection results from an evasion mechanism exhibited by CHIKV that is dependent on widespread shutoff of cellular protein synthesis and a targeted block to late synthesis of antiviral mRNA transcripts. Tanzania in 1953 (52, 69). The virus causes an acute febrile illness associated with severe joint pain that can persist long after viral clearance (9,26,42,47,49,62,68,75). In 2005 and 2006 CHIKV reemerged on a number of Indian Ocean islands and subsequently in India in 2006 and 2007 (78). Since these locations are popular tourist destinations, such outbreaks represent significant threats to European countries from travelerassociated infections. Because the virus is transmitted most commonly via mosquitoes (23, 67), changing patterns of vector distribution and abundance in response to climate change (36) and increased vector-human contact following human encroachment into undeveloped areas renders CHIKV an emerging pathogen of high potential danger for future generations. Unfortunately, information regarding many basic aspects of CHIKV molecular biology, immunology, and pathology are lacking. Chikungunya virus (CHIKV) was first isolated inCHIKV is a member of the family Togaviridae and genus Alphavirus. The enveloped virion contains an icosahedral nucleocapsid and an ϳ12-kb plus-strand single-stranded RNA genome that includes a 5Ј cap and 3Ј polyadenylation. The genome includes two open reading frames (ORFs) separately encoding polyproteins th...

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“…The females were much more affected than males because they reside in the house at daytime and may get exposed to the vector Aedes sp., which is domestic in nature and a day biter. [15][16][17] No significant difference was observed between the residents of urban/semi-urban and rural areas, although people in the urban/semi-urban areas were more affected by both monotypic and dual infection.…”

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confidence: 99%

A Comparative Study of Clinical Features between Monotypic and Dual Infection Cases with Chikungunya Virus and Dengue Virus in West Bengal, India

Taraphdar¹,

Sarkar²,

Mukhopadhyay³

et al. 2012

The American Society of Tropical Medicine and Hygiene

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Chikungunya virus (CHIKV) and dengue virus (DENV) are circulating individually in the state of West Bengal, India. However, after 1965 the dual-infection caused by both viruses had not been recorded until 2010. In 2010, an investigation of the febrile cases was carried out to confirm the involvement of both viruses simultaneously. A total of 550 blood samples were tested for the detection of immunoglobulin M (IgM) antibody against both CHIKV and DENV. Serology by the enzyme-linked immunosorbent assay method confirmed that 131 (23.8%) and 104 (18.9%) patients had IgM antibody against CHIKV and DENV, respectively, whereas 68 (12.4%) had IgM antibodies against both CHIKV and DENV. Fever, joint pain, rashes, headache, myalgia, and nausea/vomiting are the common features in the case of both monotypic and dual-infection. Severe arthralgia and swelling of joints were common only in CHIKV-positive cases and abdominal pain was mainly associated with DENV infection. Diarrhea was reported only by the dual-infected patients (16.2%).

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Resurgence of chikungunya virus in India: an emerging threat

Abstract: Since December 2005, an outbreak of chikungunya virus (CHIKV) infection has been ongoing in various states of India

Cited by 35 publications

References 5 publications

Tracking epidemic Chikungunya virus into the Indian Ocean from East Africa

Tracking epidemic Chikungunya virus into the Indian Ocean from East Africa

Chikungunya Virus Induces IPS-1-Dependent Innate Immune Activation and Protein Kinase R-Independent Translational Shutoff

A Comparative Study of Clinical Features between Monotypic and Dual Infection Cases with Chikungunya Virus and Dengue Virus in West Bengal, India

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