**1. Introduction**

The apicomplexan parasite *Plasmodium*, which is accountable for malaria, has a complex life cycle that includes both vertebrate hosts and invertebrate mosquitoes. Adaptation to blood-feeding in mosquitoes has made it inadvertently a carrier of various diseases. A blood meal is indispensable for adult female mosquitoes to nourish its egg, and maintain the gonotrophic cycle. But during blood feeding, ingestion of *Plasmodium* gametocyte from an infected person's blood results in the onset of 18-20 days long sporogonic cycle that culminates in the production of infectious sporozoites in the mosquito host [1]. These infectious sporozoites are then delivered into the human body through salivary discharge, which initiates the intricate stages of the asexual process causing malaria. In humans, malaria is caused by five *Plasmodium* species i.e*., Plasmodium falciparum, P. vivax, P. malariae, P. ovale,* and *P. knowlesi* [2]*.*

*P. falciparum* and *P. vivax*, vectored by the adult female *Anopheline* mosquitoes, are two principal parasites of human malaria [3]. Of the five *Plasmodium* species that cause human malaria, *Plasmodium vivax* is the most geographically widespread [4]. The parasite could survive quiescent for extended periods when circumstances

are not conducive to its ongoing transmission [5]. According to the current report by WHO, in the year 2019 around 75% of malaria cases were caused by *P. vivax* in the WHO Region of the Americas. An approximated 52% of the global burden of *P. vivax* emerged from the WHO South-East Asia Region, among which 47% were contributed from India [6].

*P. vivax* is considered as a less fatal parasite, but the recent emergence of more *P. vivax* infected cases in *P. falciparum* endemic areas, and increased mortality, morbidity rates are drawing our attention to this least studied parasite. It is more difficult to monitor and eradicate the *P. vivax* than *P. falciparum*, because of limited information, and associated biological complexities of its development in the mosquito as well as the human host [7, 8].

*P. vivax* normally circulates at low peripheral parasite densities, but still, they are transmissible by the mosquito vectors, and hence presents major challenges for the diagnosis of infected peoples. *P. vivax* has adapted to live with varying *Anopheles* vectors in different ecological conditions. Unlike other *Plasmodium* species, *P. vivax* has the potential to form dormant hypnozoites inside the host liver, and these liver-stage parasites are accountable for malaria relapses for weeks or months after initial infection [5]. Lastly, the lack of long-term *in-vitro* culture further restricts our understanding of the biological consequences of *P. vivax* development and transmission [9]. Nevertheless, for the last two decades, the integration and utilization of high-throughput molecular technologies such as genomics, RNA-Seq/transcriptomics, proteomics, have been valuable to decode and trace the genetic variation and diversity in the *P. vivax* population collected from different geographical origins [10, 11]. Efforts are continuing to uncover molecular and functional correlation of tissue/stage-specific *P. vivax* biology in the vertebrate host, identify genetic signatures to develop new diagnosis tools, anti-*P. vivax* drugs, or vaccine development. However, the biological complexity of the *P. vivax* development cycle in the mosquito vector-host is too limited, and therefore in this article, we highlight the current progress made so far in the understanding of the Mosquito-*P. vivax* interaction biology.
