In:
eLife, eLife Sciences Publications, Ltd, Vol. 4 ( 2015-08-18)
Kurzfassung:
Human Immunodeficiency Virus (HIV) is a sexually transmitted virus that can cause a serious disease that weakens the immune system. The virus is most commonly transmitted between individuals in semen, the male reproductive fluid. Semen contains deposits of protein fragments called amyloid fibrils, which can increase the transmission of HIV by trapping viral particles. This helps the virus to attach to the membranes surrounding human cells, which increases the risk of infection. Therefore, therapies that reduce the levels of amyloid fibrils in semen might be able to reduce the transmission of HIV. Drugs that prevent amyloid formation are already being developed because structurally similar fibrils can also form in the brains of individuals with neurodegenerative diseases. One such molecule—called CLR01—works by binding to particular sites on the proteins that form fibrils in the brain. This inhibits fibril formation and slowly disassembles the fibrils that have already formed. CLR01 physically interacts with these residues in a way that resembles a tweezer. The peptides in the amyloid fibrils in semen also have these sites, which suggests that CLR01 might also disrupt amyloid fibrils from forming in semen. Here Lump and Castellano et al. show that CLR01 can both disrupt fibril formation and remodel fibrils that have already formed. In addition, CLR01 prevents HIV particles from interacting with these fibrils and can displace the virus particles that have already bound to the fibrils. In the presence of CLR01, human cells exposed to semen that contained HIV were less likely to become infected with the virus. Unexpectedly, CLR01 also directly destroys HIV and other enveloped viruses such as HCV or HSV particles by disrupting the membranes that surround the virus. Therefore, Lump and Castellano et al.'s findings reveal that CLR01 has considerable potential to be used as an agent for reducing the transmission of HIV and other sexually transmitted viral diseases.
Materialart:
Online-Ressource
ISSN:
2050-084X
DOI:
10.7554/eLife.05397.001
DOI:
10.7554/eLife.05397.002
DOI:
10.7554/eLife.05397.003
DOI:
10.7554/eLife.05397.004
DOI:
10.7554/eLife.05397.005
DOI:
10.7554/eLife.05397.006
DOI:
10.7554/eLife.05397.007
DOI:
10.7554/eLife.05397.008
DOI:
10.7554/eLife.05397.009
DOI:
10.7554/eLife.05397.010
DOI:
10.7554/eLife.05397.011
DOI:
10.7554/eLife.05397.012
DOI:
10.7554/eLife.05397.013
DOI:
10.7554/eLife.05397.014
DOI:
10.7554/eLife.05397.015
DOI:
10.7554/eLife.05397.016
DOI:
10.7554/eLife.05397.017
DOI:
10.7554/eLife.05397.018
DOI:
10.7554/eLife.05397.019
DOI:
10.7554/eLife.05397.020
DOI:
10.7554/eLife.05397.021
DOI:
10.7554/eLife.05397.022
DOI:
10.7554/eLife.05397.023
DOI:
10.7554/eLife.05397.024
DOI:
10.7554/eLife.05397.025
DOI:
10.7554/eLife.05397.026
DOI:
10.7554/eLife.05397.027
DOI:
10.7554/eLife.05397.028
DOI:
10.7554/eLife.05397.029
DOI:
10.7554/eLife.05397.030
DOI:
10.7554/eLife.05397.031
DOI:
10.7554/eLife.05397.032
Sprache:
Englisch
Verlag:
eLife Sciences Publications, Ltd
Publikationsdatum:
2015
ZDB Id:
2687154-3
