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科学: 新药能治疗几乎所有病毒性感染 [复制链接]

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发表于 2011-8-10 21:30 |只看该作者 |倒序浏览 |打印
本帖最后由 风雨不动 于 2012-4-14 14:57 编辑

绝大多数细菌性感染可用抗生素如青霉素治疗,然而抗生素药物对于病毒性感染如普通感冒、流行性感冒、出血热和埃博拉病毒等,毫无用处。现在,MIT林肯实验室的研究人员设计出新的药物,能识别出被病毒感染的细胞,然后杀死细胞终止感染。研究报告发表在PLoS One上。 研究人员测试了15种病毒,发现新药物能有效对付所有这些病毒——包括引起普通流感的鼻病毒,H1N1流感病毒,胃病毒,脊髓灰质炎病毒,登革热和出血热病毒。药物针对的是病毒感染的细胞所产生的某种独特RNA。发明这项技术的Todd Rider表示,在理论上,该药物对所有病毒都有效。

http://web.mit.edu/newsoffice/2011/antiviral-0810.html
New drug could cure nearly any viral infectionResearchers at MIT’s Lincoln Lab have developed technology that may someday cure the common cold, influenza and other ailments.
Anne Trafton, MIT News Office



today's newsOn thin ice
Taken from the Canadian Research Icebreaker CCGS Amundsen, in the Beaufort Sea in September 2009.
Photo: V. Dansereau

The most recent global climate report fails to capture the reality of the changing Arctic seascape, according to MIT researchers.



August 10, 2011



Most bacterial infections can be treated with antibiotics such as penicillin, discovered decades ago. However, such drugs are useless against viral infections, including influenza, the common cold, and deadly hemorrhagic fevers such as Ebola.

Now, in a development that could transform how viral infections are treated, a team of researchers at MIT’s Lincoln Laboratory has designed a drug that can identify cells that have been infected by any type of virus, then kill those cells to terminate the infection.


The microscope images above show that DRACO successfully treats viral infections. In the top set of four photos, rhinovirus (the common cold virus) kills untreated human cells (lower left), whereas DRACO has no toxicity in uninfected cells (upper right) and cures an infected cell population (lower right). Similarly, in the bottom set of four photos, dengue hemorrhagic fever virus kills untreated monkey cells (lower left), whereas DRACO has no toxicity in uninfected cells (upper right) and cures an infected cell population (lower right). | Enlarge image

In a paper published July 27 in the journal PLoS One, the researchers tested their drug against 15 viruses, and found it was effective against all of them — including rhinoviruses that cause the common cold, H1N1 influenza, a stomach virus, a polio virus, dengue fever and several other types of hemorrhagic fever.

The drug works by targeting a type of RNA produced only in cells that have been infected by viruses. “In theory, it should work against all viruses,” says Todd Rider, a senior staff scientist in Lincoln Laboratory’s Chemical, Biological, and Nanoscale Technologies Group who invented the new technology.

Because the technology is so broad-spectrum, it could potentially also be used to combat outbreaks of new viruses, such as the 2003 SARS (severe acute respiratory syndrome) outbreak, Rider says.

Other members of the research team are Lincoln Lab staff members Scott Wick, Christina Zook, Tara Boettcher, Jennifer Pancoast and Benjamin Zusman.

Few antivirals available

Rider had the idea to try developing a broad-spectrum antiviral therapy about 11 years ago, after inventing CANARY (Cellular Analysis and Notification of Antigen Risks and Yields), a biosensor that can rapidly identify pathogens. “If you detect a pathogenic bacterium in the environment, there is probably an antibiotic that could be used to treat someone exposed to that, but I realized there are very few treatments out there for viruses,” he says.

There are a handful of drugs that combat specific viruses, such as the protease inhibitors used to control HIV infection, but these are relatively few in number and susceptible to viral resistance.  

Rider drew inspiration for his therapeutic agents, dubbed DRACOs (Double-stranded RNA Activated Caspase Oligomerizers), from living cells’ own defense systems.

When viruses infect a cell, they take over its cellular machinery for their own purpose — that is, creating more copies of the virus. During this process, the viruses create long strings of double-stranded RNA (dsRNA), which is not found in human or other animal cells.

As part of their natural defenses against viral infection, human cells have proteins that latch onto dsRNA, setting off a cascade of reactions that prevents the virus from replicating itself. However, many viruses can outsmart that system by blocking one of the steps further down the cascade.

Rider had the idea to combine a dsRNA-binding protein with another protein that induces cells to undergo apoptosis (programmed cell suicide) — launched, for example, when a cell determines it is en route to becoming cancerous. Therefore, when one end of the DRACO binds to dsRNA, it signals the other end of the DRACO to initiate cell suicide.

Combining those two elements is a “great idea” and a very novel approach, says Karla Kirkegaard, professor of microbiology and immunology at Stanford University. “Viruses are pretty good at developing resistance to things we try against them, but in this case, it’s hard to think of a simple pathway to drug resistance,” she says.

Each DRACO also includes a “delivery tag,” taken from naturally occurring proteins, that allows it to cross cell membranes and enter any human or animal cell. However, if no dsRNA is present, DRACO leaves the cell unharmed.

Most of the tests reported in this study were done in human and animal cells cultured in the lab, but the researchers also tested DRACO in mice infected with the H1N1 influenza virus. When mice were treated with DRACO, they were completely cured of the infection. The tests also showed that DRACO itself is not toxic to mice.

The researchers are now testing DRACO against more viruses in mice and beginning to get promising results. Rider says he hopes to license the technology for trials in larger animals and for eventual human clinical trials.

This work is funded by a grant from the National Institute of Allergy and Infectious Diseases and the New England Regional Center of Excellence for Biodefense and Emerging Infectious Diseases, with previous funding from the Defense Advanced Research Projects Agency, Defense Threat Reduction Agency, and Director of Defense Research & Engineering (now the Assistant Secretary of Defense for Research and Engineering).










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第一投注.现金网:招代理年薪10万以上:6668.cc

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发表于 2011-8-10 21:32 |只看该作者
本帖最后由 brucexm 于 2011-8-10 21:35 编辑

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0022572

Broad-Spectrum Antiviral Therapeutics
Abstract Top

Currently there are relatively few antiviral therapeutics, and most which do exist are highly pathogen-specific or have other disadvantages. We have developed a new broad-spectrum antiviral approach, dubbed Double-stranded RNA (dsRNA) Activated Caspase Oligomerizer (DRACO) that selectively induces apoptosis in cells containing viral dsRNA, rapidly killing infected cells without harming uninfected cells. We have created DRACOs and shown that they are nontoxic in 11 mammalian cell types and effective against 15 different viruses, including dengue flavivirus, Amapari and Tacaribe arenaviruses, Guama bunyavirus, and H1N1 influenza. We have also demonstrated that DRACOs can rescue mice challenged with H1N1 influenza. DRACOs have the potential to be effective therapeutics or prophylactics for numerous clinical and priority viruses, due to the broad-spectrum sensitivity of the dsRNA detection domain, the potent activity of the apoptosis induction domain, and the novel direct linkage between the two which viruses have never encountered.


....具体看链接


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发表于 2011-8-10 21:51 |只看该作者
求真相!

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发表于 2011-8-10 22:04 |只看该作者
要是杀死细胞,那不会把整个肝脏杀死啊

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发表于 2011-8-10 22:04 |只看该作者
对艾滋病也有效?

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发表于 2011-8-11 14:09 |只看该作者
涉及性命的慎用,

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发表于 2011-8-11 16:02 |只看该作者
乙肝病毒是DNA病毒

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才高八斗

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发表于 2011-8-11 17:16 |只看该作者
本帖最后由 StephenW 于 2011-8-11 17:18 编辑
tonychant 发表于 2011-8-11 16:02
乙肝病毒是DNA病毒

I am no expert, it seems DRACO will not work for HIV or HBV.
http://www.nature.com/ajg/journal/vaop/ncurrent/fig_tab/ajg2009726t1.html
Table 1. Characteristics of HIV, hepatitis B, and hepatitis C

HIVHBVHCV
StructuressRNAPartially dsDNAssRNA
Genome length9.8
kb
3.2
kb
9.4
kb
Replication sequencessRNA → dsDNA → integration → ssRNAPartial dsDNA → minus-strand dsDNA → pregenomic RNA → minus-strand RNA → positive-strand DNA → partial dsDNAssRNA → dsRNA → ssRNA
Entry moleculeHIV gp/20 + CD4, HIV gp 41 + cxcR4 or CCR5UnknownHCV envelope glycoproteins + (Claudin-1, occludin-1, CD81, SRB1)
Viral proteins involved in replicationProtease, reverse transcriptase, integrase, virion infectivity factor (vif): vpr, vpu, tat, hef, rev, vpxEnl, Enll, post-transcription regulatory element (PRE)NS5B + NS proteins in the replication complex
Steps inhibited by current drugs243Approx. 6
Integration into host DNAYesNo, episomal formNo
Location of mature virion assemblyCell membraneCytoplasmCytoplasm
Principal host cellCD4 + T-cellHepatocyteHepatocyte
Half-life, infected cell17
h
Weeks–monthsWeeks–months
Half-life, free virus45
min
3–24
h
3
h
Virions produced per day1091012–10131012–1013
dsDNA, double-stranded DNA; dsRNA, double-stranded RNA; HBV, hepatitis B virus; HCV, hepatitis C virus; NS, non-structural protein; ssRNA, single-stranded RNA.

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