In order to be able to ward off disease pathogens, immune cells must be mobile and be able to establish contact with each other.

The working group around Professor Dr. Oliver Fackler in the Virology Department of the Hygiene Institute of the Heidelberg University Hospital has discovered a mechanism in an animal model revealing how HIV, the AIDS pathogen, cripples immune cells: Cell mobility is inhibited by the HIV Nef protein.

The human immunodeficiency virus (HIV) has developed numerous strategies for eluding the body's defenses and the medications administered. The prerequisite for efficient reproduction of the virus in the patient’s body is the virus’s own Nef protein.

Without Nef, the development of AIDS is significantly slowed or even stopped completely. The underlying mechanism of this observation was a complete mystery up to now, however.

HIV modifies the cell structure system of the host cells

Viruses alter the support structures of affected cells, enabling them to enter the cells more easily. The cell structure element actin, which also gives muscles their mobility, aids in the motility of immune cells. This is necessary for immune cells to be able to establish contact with each other and combat the virus. After each movement, actin must be returned to its original state in order to be available once again.

HIV especially attacks immune cells of the T-helper type. These cells support not only direct "defense against the enemy", but are also necessary for building sufficient antibodies against the invader. For this, they must rely on their mobility.

"The actin cytoskeleton of human T-lymphocytes (red) in the presence of the stimulus CCL-19. An HIV-1 infection (HIV-1 protein CA in green) leads to the loss of actin reorganization and therefore of cell motility. (Credit: Hygiene Institute, Heidelberg University Hospital)"

Source: University Hospital Heidelberg