Hantaviruses demonstrate a high variability in their ability to infect humans and in the manifestation and severity of the disease caused.

For entry, pathogenic hantaviruses use integrin 尾₃ and CD55, non-pathogenic hantaviruses use integrin 尾_1.

The identification of novel hantaviruses opens new questions regarding receptor usage and pathogenicity.

Differences in entry mechanisms may be responsible for the clinical picture.

Patient-specific determinants such as cytokine release and repair by mobilization of stem cells may also contribute to the clinical outcome.