· 博主按：無論如何，還是自己要有安全措施才是防範最好的保證，雖然最好的防範也不一定有100%的安全保證！防不勝防，小心為是，好之為之。
愛滋病病毒图。
Cell Protein Found That Literally Nips HIV In The Bud
ScienceDaily (Jan। 14, 2008) — UCLA researchers have found that a key protein in the body’s dendritic cells can stop the virus that causes AIDS from ”budding” -- part of the virus’ life cycle that is crucial to its ability to replicate and infect other cells.
”If we can block virus generation, then we can control the disease,” said lead author Shen Pang, associate professor in the division of oral biology and medicine at the UCLA School of Dentistry and a member of the UCLA AIDS Institute.
Dendritic cells are specialized white blood cells in the skin, mucosa and lymph nodes that kick-start a primary immune response to foreign invaders by activating lymphocytes, including the T cells that HIV targets. Though dendritic cells can be infected with HIV -- and indeed play a crucial role in transmitting the virus to T cells -- studies have shown that viral generation from these cells is nearly a hundred times lower than from infected T cells, indicating that the cells may possess some inhibiting property.
Pang hypothesized that DC-SIGN, a protein expressed in dendritic cells, may be responsible for such inhibition. He and his colleagues found that DC-SIGN and a related protein, DC-SIGNR, both demonstrated 95 percent to 99.5 percent inhibition of viral production from host cells.
Very few cells are infected when HIV first enters the human body, but the virus rapidly creates new copies of itself, which in turn infect more cells. To achieve this, the virus, after infecting a cell, sends envelopes of protein to the cell’s membrane. The viral genomes then combine with viral structural proteins and move into these envelopes. The envelopes bubble, or bud, outward, releasing viral particles that will infect more cells and start new viral life cycles.
According to the researchers, DC-SIGN appears to block HIV generation by efficiently neutralizing an HIV glycoprotein on the surface of the HIV envelope known as gp120, a key to viral infection. In such cases, while some viral particles may still be released from the infected dendritic cells, the lack of gp120 in their envelopes means they are not infectious to CD4-positive T-lymphocytes and macrophages. In other words, these viral particles have been rendered uninfectious.
Current methods to interrupt the life cycle of the virus are limited because they generally target HIV at the stages of viral entry, reverse transcription and post-translational protein cleavages. Once the virus passes through these stages, treatment fails. The UCLA researchers, therefore, focused on halting the virus’ generation at different stages in its life cycle.
”The strong inhibition of viral production by DC-SIGN suggests the possibility of using this protein for treatment of HIV-infected patients,” the researchers write. ”Expression of this protein in various CD4-positive cells should inhibit viral production from infected cells. Because it can also enhance the immune response, DC-SIGN is expected to be useful for in vivo studies for developing an HIV vaccine.”
The study, scheduled for publication in the April issue of the Federation of American Societies for Experimental Biology’s FASEB Journal and may be available online at http://www.fasebj.org/cgi/rapidpdf/fj.07-9443comv3.pdf. Pang’s co-author is Qiuwei Wang, a postgraduate researcher in the division of oral biology and medicine at the UCLA School of Dentistry.
This study was supported by the UCLA AIDS Institute, the UCLA School of Dentistry and a grant from the National Institutes of Health.
Adapted from materials provided by University of California - Los Angeles, via EurekAlert!, a service of AAAS.
Via CCR5
以防万一中了镖！
安全带上 一路平安！ 安全套上 坐怀不乱！
螳螂捕蝉， 黄雀在后！
।sina.com.cn/s/blog_5068657301009ipy.html">http://blog।sina.com.cn/s/blog_5068657301009ipy.html
1 条评论:
不錯健康保帖…^^
发表评论