Abstract
Visceral leishmaniasis (VL) is a widely spread zoonotic disease. In Brazil the disease is caused by Leishmania (Leishmania)infantum chagasi. Peridomestic sandflies acquire the etiological agent by feeding on blood of infected reservoir animals, such as dogs or wildlife. The disease is endemic in Brazil and epidemic foci have been reported in densely populated cities all over the country. Many clinical features of Leishmania infection are related to the host-parasite relationship, and many candidate virulence factors in parasites that cause VL have been studied such as A2 genes. The A2 gene was first isolated in 1994 and then in 2005 three new alleles were described in Leishmania (Leishmania) infantum. In the present study we amplified by polymerase chain reaction (PCR) and sequenced the A2 gene from the genome of a clonal population of L. (L.) infantum chagasi VL parasites. The L. (L.) infantum chagasi A2 gene was amplified, cloned, and sequenced in. The amplified fragment showed approximately 90% similarity with another A2 allele amplified in Leishmania (Leishmania) donovani and in L. (L.) infantum described in literature. However, nucleotide translation shows differences in protein amino acid sequence, which may be essential to determine the variability of A2 genes in the species of the L. (L.) donovani complex and represents an additional tool to help understanding the role this gene family may have in establishing virulence and immunity in visceral leishmaniasis. This knowledge is important for the development of more accurate diagnostic tests and effective tools for disease control.
Highlights
Visceral leishmaniasis (VL) is widespread in tropical and subtropical areas of Latin America, Europe, Africa and Asia
The present study describes an A2 allele found in a L. (L.) infantum chagasi strain, isolated from a dog with VL treated in the Veterinary Hospital of Universidade Estadual Paulista in the city of Jaboticabal, São Paulo, Southeastern Brazil
The accession number for the A2 gene isolated in L. (L.) infantum chagasi described in this study is [GenBank:GQ290460]; the accession numbers for L.(L.)infantum A2 alleles II, III, and IV are [GenBank:AY255807, GenBank: AY255808, and GenBank: AY255809], respectively (GARIN et al, 2005), and the accession number for L. (L.) donovani is [GenBank:S69693] (CHAREST; MATLASHEWSKI, 1994)
Summary
Visceral leishmaniasis (VL) is widespread in tropical and subtropical areas of Latin America, Europe, Africa and Asia. Among candidate virulence factors in parasites that cause VL are the A2 genes (ZHANG; MATLASHEWSKI, 1997, 2001). (L.) donovani are composed predominantly of a sequence encoding 10 amino acids that may be repeated 40 to 90 times depending on each specific gene (CHAREST; MATLASHEWSKI, 1994; GHOSH; ZHANG; MATLASHEWSKI, 2001). A2 genes share similarities with the S antigen expressed by Plasmodium falciparum (CHAREST; MATLASHEWSKI, 1994), and a possible role for the structure/functionality of A2 genes in the cutaneous or visceral tropism of Leishmania parasites in L. major and L. (L.) infantum chagasi, and New World cutaneous leishmaniasis (CL), L. mexicana and L. amazonensis, have A2 genes in their chromosomes (GHEDIN et al, 1997). (L.) donovani A2 gene in this species allowed its survival in visceral organs of mice (ZHANG et al, 2003). The amplified fragment showed approximately 90% similarity with another A2 allele amplified in L. (L.) donovani (CHAREST; MATLASHEWSKI, 1994) and L. (L.) infantum (GARIN et al, 2005)
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