The proteins encoded by genes on the pathogenicity islands found in many enteric bacteria are defined as
virulence factors for primary pathogens. There are
several lines of argument for what real virulence factors
are in C. albicans, an opportunistic pathogen. They are
as follow: “all traits required to establish disease” [3],
“factors that interact directly with mammalian host cells”
[5], and “a component of a pathogen that damages the
host” [6]. In order to establish an infection, opportunistic
pathogens have to evade the immune system, survive
and divide in the host environment and spread to new
tissues. Candida spp. colonize and/or cause diseases at
several anatomically distinct sites with unique
physiological environment including skin, oral cavity
and esophagus, gastrointestinal tract, vagina, and
vascular system. C. albicans expresses PHR1 in
bloodstream or in tissues to adapt the neutral pH, while
it expresses RPH2 in vaginal canal to survive at acid
pH [7,8]. The homologues of PHR1 and PHR2 in
Candida dubliniensis have been cloned and their
functions are similar to that in C. albicans [9]. EPD1, 2
of Candida maltosa are similar in sequence to PHR1, 2
of C. albicans . Epdlp could be involved in cell wall
maintenance and is essential for pseudohyphal growth.
The transcription of EPD2 is induced strongly when cells
are grown in SD medium of higher pH (pH 7), but not
in SD medium of lower pH (pH 4) [10]. Although the
infections caused by non-albicans Candida species have
increased, C. albicans is still the most common pathogen
among fungal pathogens and has been established for
the molecular study. This review focuses on genes for
adhesion, proteinases secretion, hyphal formation, and
phenotypic switching in C. albicans