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Review
. 2022 Sep 20;14(10):2088.
doi: 10.3390/v14102088.

The Role of Mosquito Hemocytes in Viral Infections

Victor Cardoso-Jaime  1 , Chinmay Vijay Tikhe  1 , Shengzhang Dong  1 , George Dimopoulos  1
Affiliations
Review

The Role of Mosquito Hemocytes in Viral Infections

Victor Cardoso-Jaime et al. Viruses. .

Abstract

Insect hemocytes are the only immune cells that can mount a humoral and cellular immune response. Despite the critical involvement of hemocytes in immune responses against bacteria, fungi, and parasites in mosquitoes, our understanding of their antiviral potential is still limited. It has been shown that hemocytes express humoral factors such as TEP1, PPO, and certain antimicrobial peptides that are known to restrict viral infections. Insect hemocytes also harbor the major immune pathways, such as JAK/STAT, TOLL, IMD, and RNAi, which are critical for the control of viral infection. Recent research has indicated a role for hemocytes in the regulation of viral infection through RNA interference and autophagy; however, the specific mechanism by which this regulation occurs remains uncharacterized. Conversely, some studies have suggested that hemocytes act as agonists of arboviral infection because they lack basal lamina and circulate throughout the whole mosquito, likely facilitating viral dissemination to other tissues such as salivary glands. In addition, hemocytes produce arbovirus agonist factors such as lectins, which enhance viral infection. Here, we summarize our current understanding of hemocytes' involvement in viral infections.

Keywords: antiviral; hemocytes; immunity; mosquito; virus; virus dissemination.

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Conflict of interest statement

The authors declare that they have no conflict of interest.

Figures

Figure 1
Figure 1
Hemocytes’ immune response during viral infections. Hypothetical model of possible functions of hemocytes during viral infection. Blood meal contains viruses that trigger the production of digestive enzymes and midgut distention, which disrupt cellular junctions and cause apoptosis in midgut epithelium cells (gray square cells). These effects facilitate virus dissemination, allowing infection of cells and trachea via gaps in the cellular junctions and via apoptosis of cells. Viruses released from the midgut epithelium can be freely transported in the hemolymph or by infected hemocytes (circular purple (uninfected) and pink cells (infected)) that are distributed in the flowing hemolymph to secondary tissues, such as fat bodies and salivary glands, which receive the virus through the tracheal system. Hemocytes can facilitate the entry of a virus into cells of various tissues through the production of mosquito galactose-specific C-type lectins (mosGCTLs) and protein tyrosine phosphatases (mosPTPs). However, hemocytes also produce phenoloxidase (PO), antimicrobial peptides (AMPs), and thioester-containing proteins (TEPs), which are involved in virus elimination. In addition, in the later stages of infection, hemocytes take up free viruses by endocytosis or phagocytosis of apoptotic cells, together with cellular debris containing virus and dsRNA; they then develop viral small interfering RNAs (vsRNAs) that are released by exosome-like vesicles (ELVs) to enter infected cells and confer virus resistance through the RNAi pathway. Finally, hemocytes can also eliminate viruses by autophagy.
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