AIDS: envelope research update.AIDS: Envelope research update
Two published reports dealing with the structure and function of the AIDS virus AIDS virus
See HIV. , a retrovirus retrovirus, type of RNA virus that, unlike other RNA viruses, reproduces by transcribing itself into DNA. An enzyme called reverse transcriptase allows a retrovirus's RNA to act as the template for this RNA-to-DNA transcription. known as HIV HIV (Human Immunodeficiency Virus), either of two closely related retroviruses that invade T-helper lymphocytes and are responsible for AIDS. There are two types of HIV: HIV-1 and HIV-2. HIV-1 is responsible for the vast majority of AIDS in the United States. , are providing some hope -- and some cautions -- about the possibility of stemming the virus' infectivity.
Researchers at Stanford University Medical Center Stanford University Medical Center (Stanford Hospital & Clinics) is one of four hospitals affiliated with Stanford University and Stanford University School of Medicine, along with the Lucile Packard Children's Hospital, the Veteran's Administration Hospital in Palo Alto, and Santa report in the April 8 CELL that they have inhibited HIV infection in cultured cells by making a minor rearrangement of the HIV envelope protein. The envelope protein, called gp160, is normally cleaved cleaved (klevd) split or separated, as by cutting. into two pieces during virual replication inside white blood cells White blood cells
A group of several cell types that occur in the bloodstream and are essential for a properly functioning immune system.
Mentioned in: Abscess Incision & Drainage, Bone Marrow Transplantation, Complement Deficiencies . Only after the protein is cleaved into gp120 and gp41 components is the AIDS virus able to bind to to contract; as, to bind one's self to a wife s>.
See also: Bind and inflect in·flect
v. in·flect·ed, in·flect·ing, in·flects
1. To alter (the voice) in tone or pitch; modulate.
2. Grammar To alter (a word) by inflection.
3. other white blood cells. Under the direction of Joseph M. McCune, the stanford researchers made a specific mutation in the gp160 protein. In doing so, they prevented enzymatic splitting of the protein into its component pieces, rendering the virus biologically inactive.
The research supports the notion that a drug capable of blocking enzymaic splitting of gp160 inside a cell might inhibit HIV's infectivity. Along similar lines, the researchers note, custom-designed antibodies directed against gp41 or gp 120 after enzymatic splitting might also prove effective, since those pieces appear critical to infectivity. Previous research on other retroviruses had suggested such approaches to blocking infectivity might work, but the work had not been done on HIV.
Other research, however, appearing in the April 9 LANCET, strikes a cautionary note for scientists who are developing such antibodies or are developing vaccines that would stimulate the production of such antibodies. Researchers at Vanderbilt University School of Medicine report they have partially characterized two components in HIV-positive blood serum -- one of them apparently an HIV-induced antibody -- that together enhance rather than deter infection by the HIV virus. The researchers reported preliminary evidence of one such factor last year.
In the latest research, the scientists describe the presence of a suspected immunoglobulin that they believe is an antibody to some part of the HIV virus, and a second factor they say is likely to be complement--a biological compound that often interacts with antibodies to destroy cells. Together, they hypothesize hy·poth·e·size
v. hy·poth·e·sized, hy·poth·e·siz·ing, hy·poth·e·siz·es
To assert as a hypothesis.
To form a hypothesis. , these two factors might work to enhance HIV infection.
It is still not clear which part of the AIDS virus might stimulate the production of such an infection-enhancing antibody, the say, adding that vaccine developers will have to be careful to choose parts of the AIDS virus that will stimulate production of protective antibodies exclusively.
They conclude that if part of the AIDS virus "can be correlated with the induction of antibodies that together with complement enhance HIV-1 infection, then candidate vaccines should obviously be devoid of such antigenic stimuli. Those vaccines already being tested should be evaluated for their ability to stimulate infection-enhancing antibody formation."