Leptospirosis is a widespread zoonosis that frequently occurs in tropical and subtropical countries. Leptospira enters the host through
wounds or mucous membranes and spreads to the whole body through the blood, causing systemic
infection. Kidneys are the preferential site where Leptospira accumulates, especially in the renal interstitium and renal tubule epithelial cells. Clinical symptoms in humans include high
fever,
jaundice,
renal failure, and severe
multiple-organ failure (Weil's syndrome). Surface-exposed
antigens are located at the outermost layer of Leptospira and these potential
virulence factors are likely involved in primary host-pathogen interactions, adhesion, and/or invasion. Using the knockout/knockdown techniques to the evaluation of pathogenicity in the
virulence factor are the most direct and effective methods and many
virulence factors are evaluated including
lipopolysaccharides (LPS), Leptospira
lipoprotein 32 (LipL32), Leptospira ompA domain protein 22 (Loa22), LipL41, LipL71, Leptospira
immunoglobulin-like repeat A (LigA), LigB, and LipL21. In this review, we will discuss the structure, functions, and dynamics of these
virulence factors and the roles of these
virulence factors in Leptospira pathogenicity. In addition, a
protein family with special
Leucine-rich repeat (LRR) will also be discussed for their vital role in Leptospira pathogenicity. Finally, these surface-exposed
antigens are discussed in the application of the diagnosis target for
leptospirosis and compared with the serum microscope agglutination test (MAT), the gold standard for
leptospirosis.