Editing Apoptosis (section)

===HIV progression===
The progression of the [[human immunodeficiency virus]] infection into [[AIDS]] is due primarily to the depletion of [[T helper cell|CD4+ T-helper lymphocytes]] in a manner that is too rapid for the body's bone marrow to replenish the cells, leading to a compromised immune system. One of the mechanisms by which T-helper cells are depleted is apoptosis, which results from a series of biochemical pathways:<ref name="Judie">{{cite journal | vauthors = Alimonti JB, Ball TB, Fowke KR | title = Mechanisms of CD4+ T lymphocyte cell death in human immunodeficiency virus infection and AIDS | journal = The Journal of General Virology | volume = 84 | issue = Pt 7 | pages = 1649–1661 | date = July 2003 | pmid = 12810858 | doi = 10.1099/vir.0.19110-0 | doi-access = free }}</ref>
# HIV enzymes deactivate anti-apoptotic ''Bcl-2''. This does not directly cause cell death but primes the cell for apoptosis should the appropriate signal be received.  In parallel, these enzymes activate proapoptotic ''procaspase-8'', which does directly activate the mitochondrial events of apoptosis.
# HIV may increase the level of cellular proteins that prompt Fas-mediated apoptosis.
# HIV proteins decrease the amount of [[CD4]] glycoprotein marker present on the cell membrane.
# Released viral particles and proteins present in extracellular fluid are able to induce apoptosis in nearby "bystander" T helper cells.
# HIV decreases the production of molecules involved in marking the cell for apoptosis, giving the virus time to replicate and continue releasing apoptotic agents and virions into the surrounding tissue.
# The infected CD4+ cell may also receive the death signal from a cytotoxic T cell.

Cells may also die as direct consequences of viral infections. HIV-1 expression induces tubular cell G2/M arrest and apoptosis.<ref>{{cite journal | vauthors = Vashistha H, Husain M, Kumar D, Yadav A, Arora S, Singhal PC | title = HIV-1 expression induces tubular cell G2/M arrest and apoptosis | journal = Renal Failure | volume = 30 | issue = 6 | pages = 655–664 | year = 2008 | pmid = 18661417 | doi = 10.1080/08860220802134672 | s2cid = 25787186 | doi-access =  }}</ref>  The progression from HIV to AIDS is not immediate or even necessarily rapid; HIV's cytotoxic activity toward CD4+ lymphocytes is classified as AIDS once a given patient's CD4+ cell count falls below 200.<ref>{{cite web |author=Indiana University Health |url=http://iuhealth.org/riley/infectious-diseases/hiv/aids-defining-criteria/ |title=AIDS Defining Criteria &#124; Riley |publisher=IU Health |access-date=2013-01-20 |archive-url=https://web.archive.org/web/20130526052627/http://iuhealth.org/riley/infectious-diseases/hiv/aids-defining-criteria/ |archive-date=2013-05-26 |url-status=dead }}</ref>

Researchers from Kumamoto University in Japan have developed a new method to eradicate HIV in viral reservoir cells, named "Lock-in and apoptosis." Using the synthesized compound Heptanoylphosphatidyl L-Inositol Pentakisphophate (or L-Hippo) to bind strongly to the HIV protein PR55Gag, they were able to suppress viral budding. By suppressing viral budding, the researchers were able to trap the HIV virus in the cell and allow for the cell to undergo apoptosis (natural cell death). Associate Professor Mikako Fujita has stated that the approach is not yet available to HIV patients because the research team has to conduct further research on combining the drug therapy that currently exists with this "Lock-in and apoptosis" approach to lead to complete recovery from HIV.<ref>{{cite journal | vauthors = Tateishi H, Monde K, Anraku K, Koga R, Hayashi Y, Ciftci HI, DeMirci H, Higashi T, Motoyama K, Arima H, Otsuka M, Fujita M | display-authors = 6 | title = A clue to unprecedented strategy to HIV eradication: "Lock-in and apoptosis" | journal = Scientific Reports | volume = 7 | issue = 1 | pages = 8957 | date = August 2017 | pmid = 28827668 | pmc = 5567282 | doi = 10.1038/s41598-017-09129-w | bibcode = 2017NatSR...7.8957T }}</ref>