Okay, this is curious.
HGSI news release today:
Friday June 23, 6:41 am Eastern Time
Human Genome to start testing BLys protein on humans
ROCKVILLE, Md., June 23 (Reuters) - Drug research and development company Human Genome Sciences Inc. (NasdaqNM:HGSI - news) said on Friday it will start human clinical trials of a protein that could help sufferers of a defect of the immune system.
The company said the protein, called B-lymphocyte stimulator or BLyS, is made by the human body and stimulates the production of antibodies. Antibodies recognise foreign substances and help defend the body against infection by viruses, bacteria and other microorganisms, Human Genome said.
The protein will be used to help treat Common Variable Immunodeficiency, or CVID, which is one of a group of primary immunodeficiency disorders that are characterised by increased susceptibility to infection.
The condition can cause individuals to require life-long treatment with antibodies to protect against recurrent infection, Human Genome said.
The company said the hope is that by providing BLyS to these patients, they will be able to produce their antibodies to ward off infections. The company said its plans for human clinical trials follow the U.S. Food and Drug Administration review of its Investigational New Drug application.
They are just getting started in clinical trials to see if this protein induces production of appropriate antibodies.
So first, they are testing to see if the antibodies are produced.
Second, they must then see if the antibodies, once produced, (if produced) are effective against the HIV virus.
Now, here is IMNR already much further along - and showing successful results. From the 6/21/00 release:
These data represent two-year immunological results from a Phase 2 clinical trial of REMUNE, an investigational product, currently being tested in Spain (STIR-2102). These data were presented on June 18 at the Fifth European Conference on Experimental AIDS Research (ECEAR) 2000 in Madrid, Spain. CTLs are white blood cells of the immune system (CD8 lymphocytes) capable of directly killing virus-infected cells.
...
Dr. Fernandez-Cruz reported that in the subset of patients tested for CTL activity specific to HIV, all the patients tested receiving ART plus REMUNE showed significant CTL activity specifically against the virus, while all the patients tested receiving ART plus placebo showed little or no CTL activity in the same test. In addition, a significant increase in the overall number of memory CD4 T cells and memory CD8 T cells was observed in REMUNE versus placebo groups of the subset. (Memory T cells are formed after exposure to a pathogen and increase the immune system's ability to mount a swift attack when challenged again with the same pathogen.) The proliferation of CD4 T cells in response to HIV-1 antigens as well as production of a soluble cytokine, interferon-gamma, which is a measure of helper T-CD4 cell function, was significantly higher in the ART plus REMUNE group (27 patients) compared to the ART plus placebo group (27 patients). The interferon-gamma levels were also strongly correlated with levels of anti-HIV factors secreted by CD8 T cells (such as the beta-chemokines, RANTES and MIP-1 beta).
``Helper T cell immune responses and activated CTL precursors appear to increase in the patients with length of time of vaccination. These data provide evidence that some constant level of exposure to HIV, as with a therapeutic vaccine, may be necessary to induce the immune system to generate an immune response against the virus,'' said Dr. Fernandez-Cruz. ``Of particular note,'' he continued, ``REMUNE-treated individuals had helper T cell immune responses, which most likely activated and expanded the CTLs which have the capability to kill infected cells. We hope that such anti-HIV immune responses will translate into an enhancement of viral suppression, which is important for long-term management of HIV-1.''
Background
CTLs or CD8 killer T cells are believed to play an important role in combating HIV infection by at least three different mechanisms, which may not be mutually exclusive. First, CTLs are capable of directly killing HIV-infected cells by releasing cytotoxic molecules (e.g., perforin) that lyse, or punch holes, in those cells causing them to die. Without the host's cellular machinery, HIV cannot replicate. Second, CTLs also release another set of factors that include beta chemokines (e.g., RANTES, MIP-1 alpha, MIP-1 beta) that compete with HIV particles for preferred entry sites on the surface of helper T cells, thereby thwarting the hallmark viral invasion of the helper T cell population. Finally, CTLs also release factors called cytokines that suppress the ability of the virus to replicate within an already infected host cell.
I really don't understand why this isn't getting more attention! |
