**3. Drosophila model to study highly infectious diseases**

There are at present several bacterial, fungal and viral models of infection which were successfully demonstrated to infect flies and used it to understand drug efficacy. Drosophila model of infectious disease could be very low cost model

**111**

Drosophila melanogaster: *A Robust Tool to Study Candidate Drug against Epidemic…*

to study drug efficacy in-vivo; it could help to save lives by saving time during an epidemic outbreak. Understanding the disease pathogenesis in humans and drawing out a similar model in *Drosophila melanogaster* would suggest the target genes

In the recent past several research works has been conducted to understand the immune system of *Drosophila melanogaster*. At present the immune system of *Drosophila* is a well-studied model to study infectious disease [35]. Adult flies have brain, heart, lung (spiracle), liver (fat body), kidney (renal tubule), GI tract (gut/ crop), ovary/testis and versatile circulatory system (hemocyte) [36]. Apart from physiological resemblance Drosophila has 75% genetical similarity with human disease genes, due to this fact genetically tractable model could be generated to

*Drosophila melanogaster* has a well-built immune system to withstand pathogenic

incursion, comprising of cellular, humoral and innate immunity in an effective but in simpler form than humans [37]. However, due to evolutionarily conserved immune pathways found in vertebrates and invertebrates, several components of fly immune system are homologous to humans [38]. The immune activation in flies against pathogens involves processes like recognition, coagulation, melanisation, phagocytosis, apoptosis, regulation of iron metabolism, synthesis of antimicrobial

The bacterial and fungal infection leads to the activation of dToll, Imd, Eiger (TNF family homolog) and insulin like receptors (FOXO) in *Drosophila*. The drosophila toll and Imd (immune deficiency) pathways function as innate immunity. Toll receptors in flies play an important part during viral, fungal and bacterial infection. The patterns recognition receptors (PRRs) initiate the signal in fly immune system depending on the type of pathogen upon interaction [40]. Gram positive and gram negative bacterial infection activates peptidoglycan recognition protein SA (PGRP-SA) and Gram-negative binding protein 1 (GNBP1) respectively. PGRP-SA causes proteolytic cleavage of Spatzle upon stimulation of dToll, it mediates downstream signalling of dMyD88, Tube, Pelle, and DIF (dorsalrelated immunity factor) the NF-kB homolog. Imd an intracellular signalling protein located close to the transmembrane PGRP-LE and PGRP-LC proteins, activates Relish protein to trigger autophagy and phagocytosis through ImD regulated genes by rendering cellular immunity against gram negative bacteria [41]. Toll activates the nuclear factor DIF and it promotes humoral immunity in the fat body by producing varieties of anti-microbial peptides AMPs like attacin, cecropin, drosomycin,

The fungal pathogen was found to be recognized by GNBP3 along with PGRPSA and GNBP1 it activates the drosophila toll receptors [43]. The Drosophila toll-5 (Tehao) and toll-9 plays major role during fungal infection by inducing Drosomycin gene [44]. During the preliminary stage of viral infection Drosophila toll receptor homolog of human TLR, Imd (TNF-alpha), Domeless (Jak–STAT), and RNAi plays a major role against viral infection these are components of innate immune system [45]. Similar to humans the viral glycoproteins are recognized by toll receptors like toll-4, while toll-7 dependent autophagy observed during viral infection in flies [42, 46]. Jak–STAT and Imd together mediates effective immunity against viral attack in flies [47]. The domeless-hop-stat2 pathway stimulated by upd1/2/3 activates Jak–STAT regulated genes responsible for controlling viral load; it is homologous to mammalian Jak–STAT pathway [48]. The Drosophila P53 and dP38 mediates apoptosis in

*DOI: http://dx.doi.org/10.5772/intechopen.90073*

what extent is discussed here [35].

**4. Host-pathogen interaction**

and proteins responsible for the underlying disease [35].

peptides and production of reactive oxygen species [39].

defensin, metchnikowin, diptericin and drosocin [42].

Drosophila melanogaster: *A Robust Tool to Study Candidate Drug against Epidemic… DOI: http://dx.doi.org/10.5772/intechopen.90073*

to study drug efficacy in-vivo; it could help to save lives by saving time during an epidemic outbreak. Understanding the disease pathogenesis in humans and drawing out a similar model in *Drosophila melanogaster* would suggest the target genes and proteins responsible for the underlying disease [35].

In the recent past several research works has been conducted to understand the immune system of *Drosophila melanogaster*. At present the immune system of *Drosophila* is a well-studied model to study infectious disease [35]. Adult flies have brain, heart, lung (spiracle), liver (fat body), kidney (renal tubule), GI tract (gut/ crop), ovary/testis and versatile circulatory system (hemocyte) [36]. Apart from physiological resemblance Drosophila has 75% genetical similarity with human disease genes, due to this fact genetically tractable model could be generated to what extent is discussed here [35].
