Vector competency is the vector’s susceptibility to oral infection and capability to multiply or propagate and further successful transmit the diseases parasite in a healthy individual. Various extrinsic and intrinsic factors contribute to the competence of mosquito vectors for various viral agents. Extrinsic factors such as temperature, humidity and nutrition have been shown to have a direct impact on mosquito fitness, survival, parasite development 29. Temperature is one of the key factors that affect the biology of mosquito vector and thereby influence vector life cycle, population density, adult survival and susceptibility to a viral pathogen. Studies have shown that the higher temperature fluctuation between day and night can reduce incubation period of dengue virus 30. In contrast, a spread of the virus to different body parts of mosquito was greatly reduced, when immatures were reared in cold water 31.

Humidity and precipitation are also responsible for mosquito population buildup. Precipitation results in an exponential increase in larval breeding habitats and higher humidity provide a conducive environment for the adult mosquito to survive. Changes in environmental temperature and humidity influence the extrinsic incubation period (EIP), it’s the incubation period from the time when mosquito acquires a viremic blood meal to the time when a mosquito is ready to transmit a virus to a healthy individual.

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Increase in temperature and humidity leads to the shorting of EIP and increased blood feeding frequency 32. A positive correlation has been observed in rail fall and dengue incidence in Thailand and Latin America 33,34. Another important extrinsic factor is quality and quantity of the food, which has a direct relation to mosquito fitness and survival. For instance, scarcity of food during larval stage has been reported to delay in malaria parasite development in adult Anopheles stephensi mosquito 35.There are growing agreement that midgut physiology, microbiota, mosquito immune response and genetic makeup are the intrinsic factors which influence vector competence 29. In virus transmission cycle, mosquito gut plays an important role and is a site where the virus first encounters the mosquito environment. Various physiological and biochemical changes take place in mosquito gut after blood feeding.

Reversible functional changes induced in mitochondria of Ae. aegypti females after blood feeding, which leads to a reduction in oxygen consumption and hydrogen peroxide generation during early and mid-phase of blood digestion which reaches its higher level during the late phase 36. At the molecular level, transcription factors, ion binding proteins and other metabolic proteins are upregulated in Ae. aegypti females during flavivirus infection and genes responsible for proteases and pupal cuticle proteins are downregulated 37. Mosquito Ubiquitin protein Ub3881 is highly downregulated during dengue virus infection in Ae.

aegypti females37. Ubiquitin is involved in degradation of dengue virus envelop protein leads to reduced number of virus released from an infected cell 29. Another protein, C-type lectins play a significant role in the establishment of flavivirus infection in mosquito vectors 38,39. Knockdown of mosGCTL-1 gene or administration of antimosGCTL-1 antibody has found to reduce infection of WNV in Aedes and Culex mosquito 40. Aedes aegypti midgut protein carboxypeptidase B1 (CPB1) also interact with DENV-2 envelope protein, and in the presence of CPB1, virus released from infected cells could not complete their protein assembly thus reduced the chances of salivary gland colonization 41.  Mosquito gut provides a conducive environment for the microorganism to flourish and, a wide variety of bacterial species have been isolated and identified from mosquito gut 42-44. These microorganisms can affect vector competence of mosquito either inducing host immune system or by directly interacting with virus agent 45. In some studies, the absence of midgut bacteria has resulted in enhanced vector competence of mosquito vector such as Anopheles mosquitoes that was reared on an antibiotic supplemented diet (to reduce midgut bacteria) has shown increased susceptibility to Plasmodium falciparum46.

A similar observation has been made by Xi et al, where Ae. aegypti mosquitoes have shown an increased level of dengue infection in females exposed to antibiotics 47. Presence of some bacteria species can enhance vector competence such as susceptibility to Ae. aegypti to dengue and chikungunya virus is greatly increased in presence of Serratia odorifera in mosquito gut 48,49. On the other hand, some bacterial species have shown a deleterious impact on vector competence of mosquito vector.

Plasmodium falciparum invasion in midgut epithelium is greatly reduced in presence of Enterobacter sp. in Anopheles mosquito 45.  Mosquito exerts an innate immune response on exposure to the infectious parasite. This immune response is the first line of defence against any foreign infection including arboviruses.

The JAK-STAT, Toll signalling and RNAi pathways are also major immune response elicited by arbovirus infection in mosquito vector 37,50.  Mosquito immune response reduces the viral pathogenesis during infection. Upon dengue virus infection, Ae.

aegypti females induce a Toll-mediated immune response to suppress the infection 47. Aedes aegypti mosquito also relies on RNAi mediated immune response for silencing viral gene expression upon dengue and other arbovirus infection 51. Arbovirus has to overcome these defense mechanisms to successfully complete transmission cycle in mosquito host. Another important intrinsic factor is the genetic makeup of mosquito vectors and viruses. The genetically different population of Ae. albopictus mosquito has shown differential vectorial competence for CHIKV oral infection 52. The study conducted by Mercado-Curiel and colleague (2008) has suggested a role of dengue receptor R67/R64 proteins (67 kDa protein) as a vector competence marker in Ae.

aegypti mosquito for dengue virus 53. Similarly, Ae. aegyptipopulations, differing in isozyme profiling have shown variable susceptibility to yellow fever virus 54. Different Ae. albopictus geographic strains have shown differential susceptibility to CHIV oral infection 52.



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