Vector-borne diseases(VBDs) are reported to represent amount 17% of all infectious diseases. The geographical distribution of vectors depends upon various climatic factors, and social factors. In the recent past, the spread of VBDs across the world is so rapid that it is associated with a change in climatic factors, global warming, travel and trade, unplanned urbanization, deforestation etc. Amongst the vector-borne diseases notable is West Nile fever (WNF) caused by West Nile Virus (WNV). WNF belongs to the family of Flaviviridae, which is part of the Japanese encephalitis antigenic group. WNV is transmitted from infected birds to human beings by mosquito bites. WNV is readily reported in Africa, Europe, the Middle East, North America and West Asia. Looking at the history, WNV was first isolated in a woman in the West Nile district of Uganda in 1937. It was identified in birds (crows and columbiformes) in the Nile delta region in 1953. Over the past 50 years, human cases of WNV have been reported in various countries.

The immune system is highly complex; it senses foreign invaders, thus protecting the body. The adaptive arm of the immune system confers long-term protection, whereas the innate immune system confers immediate protection. In the case of the immune system, the pattern recognition receptors offer various modes of sensing the pathogen-associated molecular patterns present in pathogens. The receptors that sense invading pathogens are called Pattern recognition receptors [1]. The adaptive immune system is very sophisticated, as it is trained to identify only the “specific antigen”, but PPRs are customised to sense a wide array of “common patterns” present in the pathogens. Cerebral pericytes are the cells that are seen as embedded in the basement membrane of capillaries. Matzinger [2] gave a new insight into the recognition of pathogens by PRRs as those that recognise PAMPs and DAMPs (Damage Associated Molecular Patterns). While PAMPs can be presented as exogenous ligands to the receptor, DAMPs are presented as endogenous ligands. Once these PRRs are activated either by PAMPs or DAMPs, they lead to the production of inflammation to clear the infection. However, over-activation during chronic conditions leads to pathological changes.

The World Health Organization (WHO) defines cerebral malaria (CM) as an otherwise unexplained coma in a patient with asexual forms of malaria parasites on the peripheral blood smear. Malaria is a severe, devastating illness characterised by respiratory distress, severe anemia, and cerebral malaria (CM). Altered consciousness, convulsions, ataxia, hemiparesis, and other neurologic and psychiatric impairments are noted in cerebral malaria. Thus, cerebral malaria is defined as a condition in which a human has Plasmodium falciparum, a parasite in peripheral blood, followed by neurological complications of any degree. CM accounts for 300,000 deaths per year, and almost any survivors there display severe neurological manifestations. Coma is the outcome of CM, which is again due to brain hypoxia due to inflammation, edema, Brain swelling, and vascular blockage, are all due to the sequestration of pRBCs in brain microvasculature [1, 2]. In Ugandan children with CM infected with P.falciparum, severe cognitive impairment, behaviour problems such as hyperactivity, inattentiveness, aggressive behaviour, loss of speech, hearing loss, blindness, and epilepsy were noted (Irdo et al. , 2010). Heme offered protective responses to ECM, by dampening the activation of microglia, astrocytes, and expression of IP10, TNFa, and IFNg [3].

Lymphatic filariasis is one of the neglected tropical diseases and also a disfiguring vector-borne disease. Parasitic nematodes such as Wuchereriabancrofti, Brugiamalayi, and Brugiatimori are the three types of parasites that cause lymphatic pathology in terms of hydrocele, lymphedema, and elephantiasis [1]. Among these three parasites, Wuchereriabancrofti is the principal parasite, which causes around 90% of infections. These nematodes impair the lymphatic system, thus leading to considerable morbidity in the affected people. The life cycle of this adult-stage lymphdwelling parasites is complex in nature. Once they start infecting the lymphatics, they cause swelling, dilatation, and thickening of lymph vessels.

Sandly bites transmit the Leishmania parasites under the skin, and the disease remains a major public health problem in infected countries. There are two types of Leishmaniasis, 1) Visceral Leishmaniasis 2) cutaneous Leishmaniasis. Among these two types, Visceral Leishmaniasis is fatal, and, if not treated, leads to mortality. It is observed that approximately 90% of cases come from India, Bangladesh, Sudan, South Sudan, Ethiopia, and Brazil. These diseases are caused by L. major, L. mexicana, L. guyanensis, L. amazonensis, L. braziliensis, and visceral Leishmaniasis by L. donovani, and L. chagasi. Experimental studies in KO of TLR2 and TLR4 have shown larger lesions and higher parasite loads upon infection with L. mexicana than the control mice [1]. Leishmania DNA is recognised as a PAMP by TLR9 [2]. These parasites are rapidly phagocytosized by neutrophils, macrophages, and dendritic cells. Different parasites of Leishmania elicit different kinds of responses in the host, which in turn depends on the genetics and immune responses of the host.

Dengue is one of the most important arboviral diseases recorded in the world. Dengue, a public health problem in tropical and subtropical countries, is spread by female Aedes mosquito bites. Among Aedes mosquitoes, Aedesaegypti is the primary vector and Aedesalbopictus is the less infective secondary vector [1]. Dengue hemorrhagic fever (DHF) is a severe form of the disease, that causes differential expression of the TLRs in dendritic cells (DCs). TLR3 and TLR9 in DCs of patients with early onset of dengue fever were unregulated, whereas in severe cases, poor expression of TLR3 and TLR9 is observed [2]. This kind of alteration in the TLR expression during dengue may alter the clinical manifestation of the disease. However, this can be considered for further research on therapeutics.

Infected mosquitoes of Aedes species spread Chikungunya fever upon the biting of the mosquitoes. Chikungunya fever first came to the limelight upon an outbreak in southern Tanzania in 1952. These days almost all countries in the world are reporting Chikungunya fever. There is no vaccine for the Chikungunya virus. The infection causes severe joint pain, nausea, vomiting, conductivities, headache, and muscle pain, followed by fever. Clinical manifestations occur after 2-7 days of the mosquito bite. This chapter addresses key issues on Chikungunya viral infection in brain cells with reference to the triggering of events associated with toll-like receptors.

West Nile Fever is transmitted by West Nile Virus (WNV), which is a single-stranded RNS flavivirus. This disease is transmitted by the bite of mosquitoes. This disease is endemic in various countries in Africa, Asia, Europe and North America [1, 2]. There is no vaccine yet for this disease which is displayed by various symptoms in humans varying from neurological squealae (encephalitis) and meningitis. Apart from this, patients report fever, headache, and myalgia as well.

Viral encephalitis is a major pathological situation. It can be caused either by DNA or RNA viruses. Japanese encephalitis belongs to the member of flavivirus and it is a mosquito-borne disease, causing viral disease. Japanese encephalitis can be prevented by a vaccine. TLR3 and TLR4 signal pathways are activated due to JE Japanese encephalitis infection. TLR3 and Retinoic acid-inducible I also participate in mediating inflammation owing to Japanese encephalitis infection. In this kind of virus infection first, the cells are infected, causing primary viremia, subsequently infecting the CNS tissues as well. More than 60% of the world's population is living in JE endemic places.