LA JOLLA—Normally when we think of viruses, from the common cold to HIV, we want to boost people’s immunity to fight them. But for scientists who develop therapeutic viruses (to, for example, target cancer cells or correct gene deficiencies) a more important question is: How do we keep people’s natural immune responses at bay? In these cases, an overenthusiastic immune response actually undermines the therapy.
LA JOLLA—Normally when we think of viruses, from the common cold to HIV, we want to boost people’s immunity to fight them. But for scientists who develop therapeutic viruses (to, for example, target cancer cells or correct gene deficiencies) a more important question is: How do we keep people’s natural immune responses at bay? In these cases, an overenthusiastic immune response actually undermines the therapy.
Salk Institute researchers discovered that inhibiting a protein called phospholipid scramblase 1 (PLSCR1) controls the infected cell’s antiviral response and provides long-term protection from immune attack and excessive inflammation. The results, described in the January 19, 2017, issue of Neuron, hold promise both for virally delivered treatments and inflammatory conditions like infections; autoimmune disorders such as lupus; or neurodegenerative diseases such as Alzheimer’s disease.
Because viruses have evolved such effective methods for finding their target and utilizing the host cells’ own molecular machinery, scientists are modifying viruses into long-lasting therapeutic vehicles that can deliver drugs to specific cells or tissues or selectively target and destroy tumors. But, since our immune systems don’t discriminate between destructive and therapeutic viruses, researchers must devise ways to keep the immune system from destroying the helpful versions.
Read more at Salk
Image Credits Salk Institute
