The exact pathogenesis of PCVD is still not exactly known. It has been agreed that PCV-2 infection is necessary, but its presence doesn't automatically equal PCVD. PCVD is a disease complex, which requires multiple components to develop.
The immune response seems to play a major role in the outcome of PCV-2 infections. Natural cases of pigs with PCVD have extensive lymphoid lesions (lymphocyte depletion and granulomatous inflammation) and altered cytokine expression patterns in peripheral blood mononuclear cells (PBMC's) and lymphoid organs.
Several key factors of the pathogenesis of PCVD are now known including:
Clinical PCVD appears to be triggered by a number of infectious and noninfectious factors. Virtually all commercially raised pigs are subclinically infected with low levels of PCV-2 (Larochelle et al., 2003; Harding, 2000) yet most remain healthy and do not develop clinical disease because triggering factors are absent. The exact mechanism(s) of the triggering factors is not known, but simultaneous infections with other pathogens including PRRS virus, Mycoplasma hyopneumoniae, swine influenza virus (SIV), and parvovirus, swine influenza virus (SIV), and parvovirus, or the absence of good production practices exacerbate clinical disease.

See History of Porcine Circoviral Disease (PCVD) and Current Western CanadianSituation by John Harding 2007 Banff Pork Seminar.
PCVD is a disease complex, which requires multiple components to develop.