World Mosquito Day

● Malaria

Malaria is a disease caused by the Plasmodium parasite that is transmitted to humans primarily through the bite of infected female Anopheles mosquitoes and is a serious global public health problem. According to the World Health Organization (WHO) in 2020, there were about 241 million cases of malaria globally that year, resulting in about 627,000 deaths, 95% of which occurred in Africa. Typical symptoms of malaria include fever, chills, sweating, general malaise, and in severe cases may cause coma, metabolic acidosis, severe anemia, acute renal failure or pulmonary edema.

Five species of Plasmodium are known to cause malaria in humans, with Plasmodium falciparum (P. falciparum) and Plasmodium vivax (P. vivax) being the main pathogens. Plasmodium falciparum is the most prevalent malaria parasite in the African region, whereas Plasmodium vivax is more common outside sub-Saharan Africa.

Malaria research has focused on the development of new antimalarial drugs and vaccines, and popular targets include CLK3, PKG, GGPPS, FRS, PRS, ACS, clRS, etc. ^[1]. In 2020, Yin Hang's team at Tsinghua University targeted the P. falciparum hexose transporter protein, PfHT1, to kill Plasmodium falciparum by starving the parasite to death ^[2].. In 2021, Lubin Jiang's group at the Shanghai Pasteur Institute of the Chinese Academy of Sciences (SPI) discovered a small molecule antimalarial drug candidate, Quesno (JL01), targeting PfHDAC1, a histone deacetylase in Plasmodium falciparum, which has entered the preclinical stage of research ^[3].

- Malaria Related Recombinant Protein

- Malaria Related Antibody

● Dengue Fever

Dengue Fever is an acute infectious disease caused by the Dengue Virus , which is transmitted to humans mainly through the bite of Aedes aegypti and Aedes albopictus mosquitoes. Common symptoms of dengue fever include high fever, severe headache, etc. In severe cases, it can develop into Dengue Hemorrhagic Fever (DHF) or Dengue Shock Syndrome (DSS).

Currently, the popular directions of dengue research are focused on the resolution of the genome and protein structure of the virus, mechanistic investigation of the host immune response, signaling pathways within the host cell, virus-host cell interactions, and the development of antidengue virus drugs and vaccines. Ramphan et al. investigated how the expression of DENV and Zika virus proteases altered the cellular lipid profile, which may affect viral replication ^[4].Shoushtari et al. used immunoinformatics combined with structural and neutralizing epitopes to design vaccine candidates against DENV serotypes ^[5]. Manocha's team proposed a multi-epitope based immunogen to induce cellular immunity against all DENV serotypes, addressing the limitations of existing vaccines ^[6]. Ylade et al. investigated the effectiveness of a single-dose DENV vaccine effectiveness, emphasizing the need for further research on vaccine strategies ^[7].

- Dengue Fever Related Recombinant Protein

- Dengue Fever Related Antibody

● Japanese Encephalitis

Japanese Encephalitis (JE) is an acute central nervous system infection caused by Japanese Encephalitis Virus (JEV), which is transmitted to humans mainly through the bite of Culex species mosquitoes. Japanese Encephalitis is predominantly endemic in Southeast Asia and the Western Pacific ^[8] and clinical symptoms can range from mild fever and headache to severe encephalitis including high fever, coma, convulsions, seizures and sometimes death.

Recent research directions in JE have focused on developing novel vaccines and antiviral drugs, exploring virus-host cell interactions, and understanding immunomodulatory mechanisms, etc. A study by Hong et al. investigated the antiviral activity of prion protein (PrPc) against the infection of JEV, highlighting the role of PrPc in the regulation of autophagic flux and its potential antiviral activity ^[9]. In addition, Zhang et al. showed that a fusion protein of actin and Fc fragments inhibited JEV replication, suggesting that this is a potential therapeutic target against the virus ^[10].

- Japanese Encephalitis Related Recombinant Protein

- Japanese Encephalitis Related Antibody

● Lymphatic Filariasis

Lymphatic Filariasis (JF), also known as elephantiasis, is caused by nematodes of the genus Brugia malayi, parasites that enter the body when infected Culex species mosquitoes bite humans. JF primarily affects the lymphatic system, resulting in swelling and deformities of the limbs, reproductive organs, and other body parts.

Current treatment options for lymphatic filariasis include combinations of drugs such as ivermectin, diethylcarbamazine and albendazole ^[11]. Where lymphatic filariasis coexists with other diseases such as onchocerciasis, UKETY et al. are evaluating the safety of drug treatments such as moxidectin and ivermectin ^[12]. In addition, LAST et al. are exploring the potential of large-scale drug administration of ivermectin as an adjunctive treatment for malaria control through a cluster randomized placebo-controlled trial ^[13].

● Zika Virus Disease

Zika Virus Disease (ZVD) is a viral disease caused by the Zika Virus, which is transmitted to humans primarily through the bite of the Aedes aegypti and Aedes albopictus mosquitoes. Clinical symptoms of Zika virus infection are usually mild and can appear days or weeks after infection. Common symptoms include fever, rash, conjunctivitis, muscle and joint pain, headache, and fatigue.

Current research on Zika virus includes its effects on pregnancy and birth defects, immune response, neurological manifestations, and diagnostic methods.Kim et al. demonstrated that Zika virus can infect the pericytes of the choroid plexus and cross the blood-brain barrier to enter the central nervous system, leading to microcephaly and neurological complications ^[14].Mercado et al. investigated the detection of Zika virus in amniotic fluid and its association with Zika related birth defects was studied ^[15]. In terms of immune response, Metz et al. emphasized the importance of the oligomeric state of the Zika virus E protein in defining a protective immune response ^[16].

● Yellow Fever

Yellow Fever is an acute viral hemorrhagic disease caused by Yellow Fever Virus (YFV). The virus belongs to the Flaviviridae family and is transmitted mainly through the bite of the Aedes aegypti mosquito. Yellow fever is predominantly endemic in Africa and South America, and clinical manifestations include early onset of fever, headache, backache, and nausea, which may progress to hemorrhagic tendencies, liver and kidney damage, and shock.

Genomic epidemiology is now being used to understand the dynamics and spatial corridors of YFV transmission, providing new insights into surveillance and control efforts ^[17]. Li et al. initial immunization with Japanese encephalitis virus (JEV) or YFV vaccine did not enhance the antibody response to Zika virus (ZIKV) after inactivated ZIKV vaccination ^[18]. Zina et al. studied ocular manifestations of flavivirus infections, including YFV, and have provided effective vaccines for YFV, dengue virus, and JEV [19]. Mantel et al.'s study using rhesus monkeys as a translational model provided insights into understanding the immune response of humans to the YFV vaccine, contributing to an understanding of the mechanisms of causation of YF disease, as well as an assessment of the vaccine's safety and efficacy ^[20].

● Chikungunya Fever

Chikungunya Fever, caused by Chikungunya Virus (CHIKV), is an arboviral disease that severely affects tropical and subtropical regions of the world ^[21]. Chikungunya fever is transmitted to humans mainly through the bite of Aedes aegypti and Aedes albopictus mosquitoes. Its clinical manifestations mainly include sudden onset of high fever, severe arthralgia, muscle pain, headache, rash and possibly nausea and vomiting.

Ballista et al. demonstrated that the TIM-1 receptor reduces CHIKV release by binding to envelope phosphatidylserine, thereby affecting viral entry into mammalian cells ^[22]. Ware et al. showed that CHIKV infection disrupts MHC-I antigen presentation via nonstructural protein 2, allowing the virus to escape from the surveillance of antiviral CD8 T cells ^[23]. A study by Jaquet et al. also examined the susceptibility of human muscle cells to CHIKV infection, showing that it was dependent on glycolytic activity and stage of differentiation ^[24].

● West Nile Fever

West Nile Fever (WNF) is a viral illness caused by West Nile Virus (WNV), a virus belonging to the Flaviviridae family, which is transmitted to humans and animals primarily through the bite of infected Culex species mosquitoes. Most people infected with WNV are asymptomatic or experience only mild symptoms, including fever, headache, body aches, nausea, and vomiting. In some cases, the virus can lead to severe neurological disorders, such as West Nile encephalitis or meningitis, which manifests as high fever, stiff neck, impaired consciousness, coma, or even death.

Currently, studies on WNV address various aspects of the virus, including epidemiology, detection methods, genetic susceptibility, and transmission dynamics. Shi et al. studied tick-borne pathogens near the Russian-Chinese border, revealing the prevalence of multiple pathogens in ticks ^[25], emphasizing the risk of co-infections. Rucci et al. carried out a serological survey in Argentina, revealing the WNV prevalence in avian populations, emphasizing the persistence of the virus in semi-arid ecosystems ^[26]. Bourdon et al. studied the genetic susceptibility of mouse strains to Zika virus, emphasizing the different outcomes of infection and the role of genetic variation in susceptibility ^[27].