There has been a small increase in HIV infections in the North East, while infections nationally have fallen.
Provisional data from the Health Protection Agency (HPA) shows 140 new cases of HIV in the North East in 2010, a rise of 4.4% over the 2009 figure.
Over the same period, the UK figure fell by 7.2% from 6,617 to 6,136.
Staff at Middlesbrough-based HIV support charity Teesside Positive Action said the rise was disappointing and called for better education.
这一医学奇迹燃起不少艾滋病病毒携带者康复的希望。对于这个治疗，英国伯明翰艾滋中心的迈克·桑阿格给予很高的评价，“这是具有重要意义的科学 研究”。桑阿格表示，在理论上已经证实这种变异基因能够抵抗艾滋病病毒，并且曾在白鼠体内试验过，但是这是首次科学家在人体上实验，证明这个基因能治疗艾 滋病。
美国艾滋病病毒医学协会前会长迈克尔·扎格认为，干细胞或骨髓移植必须要利用强力药物和放射物摧毁人体原有的免疫系统，然后输入捐献者的骨髓， 以重造一个新的免疫系统，这种疗法及其引发的并发症会提高死亡率。另外，治疗费用太高，大概需要几千万美元。更难的是，找到一个合适的、具有抗艾基因的骨 髓很困难，这一基因突变只存在于生活在北欧和西欧的高加索人中，且只占到其总人口的1%。
Tags: 愛滋病, 世界衛生組織
By RANDOLPH E. SCHMID, AP Science Writer Randolph E. Schmid, Ap Science Writer – Sun Aug 2, 2:31 pm ET WASHINGTON – A new strain of the virus that causes AIDS has been discovered in a woman from the African nation of Cameroon. It differs from the three known strains of human immunodeficiency virus and appears to be closely related to a form of simian virus recently discovered in wild gorillas, researchers report in Monday’s edition of the journal Nature Medicine. The finding “highlights the continuing need to watch closely for the emergence for new HIV variants, particularly in western central Africa,” said the researchers, led by Jean-Christophe Plantier of the University of Rouen, France. The three previously known HIV strains are related to the simian virus that occurs in chimpanzees. The most likely explanation for the new find is gorilla-to-human transmission, Plantier’s team said. But they added they cannot rule out the possibility that the new strain started in chimpanzees and moved into gorillas and then humans, or moved directly from chimpanzees to both gorillas and humans. The 62-year-old patient tested positive for HIV in 2004, shortly after moving to Paris from Cameroon, according to the researchers. She had lived near Yaounde, the capital of Cameroon, but said she had no contact with apes or bush meat, a name often given to meat from wild animals in tropical countries. The woman currently shows no signs of AIDS and remains untreated, though she still carries the virus, the researchers said. How widespread this strain is remains to be determined. Researchers said it could be circulating unnoticed in Cameroon or elsewhere. The virus’ rapid replication indicates that it is adapted to human cells, the researchers reported. Their research was supported by the French Health Watch Institute, the French National Agency for Research on AIDS and Viral Hepatitis and Rouen University Hospital. A separate paper, also in Nature Medicine, reports that people with genital herpes remain at increased risk of HIV infection even after the herpes sores have healed and the skin appears normal. Researchers led by Drs. Lawrence Corey and Jia Zhu of the Fred Hutchinson Cancer Research Center found that long after the areas where the herpes sores existed seem to be clear, they still have immune-cell activity that can encourage HIV infection. Herpes is marked by recurring outbreaks and has been associated with higher rates of infection with HIV. It had been thought that the breaks in the skin were the reason for higher HIV rates, but a study last year found that treatment of herpes with drugs did not reduce the HIV risk. The researchers tested the skin of herpes patients for several weeks after their sores had healed and found that, compared with other genital skin, from twice to 37 times more immune cells remained at the locations where the sores had been. HIV targets immune cells and in laboratory tests the virus reproduced three to five times faster in tissue from the healed sites as in tissue from other areas. “Understanding that even treated (herpes) infections provide a cellular environment conducive to HIV infection suggests new directions for HIV prevention research,” commented Dr. Anthony S. Fauci, director of the National Institute of Allergy and Infectious Disease. That study was funded by the National Institutes of Health and the Tietze Foundation. ___ On the Net: Nature Medicine: http://www.nature.com/nm
HIV-specific mucosal and cellular immunity in HIV-seronegative partners of HIV-seropositive individualsFebruary 20, 2009 at 2:36 am | Posted in hiv | Leave a comment
HIV-specific mucosal and cellular immunity was analyzed in heterosexual couples discordant for HIV status in serum and in HIV-unexposed controls. HIV-specific IgA but not IgG was present in urine and vaginal wash samples from HIV-exposed seronegative individuals (ESN), whereas both IgA and IgG were observed in their HIV-seropositive partners; antibodies were not detected in low-risk controls. Envelope protein (Env) peptide-stimulated interleukin-2 (IL-2) production by peripheral blood mononuclear cells (PBMCs) was detected in 9 out of 16 ESNs, 5 out of 16 HIV-infected patients and 1 out of 50 controls. Env peptide-stimulated PBMCs of ESNs produced more IL-2 and less IL-10 compared with those of HIV-infected individuals; no differences were observed in chemokine production or in CCR5 expression. These data demonstrate that a compartmentalized immune response to pathogens is possible in humans and raise the possibility of protective roles for cell-mediated immunity and mucosal IgA in HIV-seronegative individuals exposed to HIV.
Seronegative HIV-1 infection appears to be caused by an inability of the host to form HIV-1-specific antibodies, rather than to a highly virulent strain of the virus as has been suggested in the past, investigators in Portugal report.
Dr. Ana R. Cardoso, at Hospital Nossa Senhora da Craca in Tomar, and associates treated a woman who presented in 2001 with fever, malaise, anorexia and oral thrush. Serological testing in 1997 and 1999 had yielded negative results, as were those performed in October, November and December.
The diagnosis was made in December based on the detection of p24 antigen and HIV-1 RNA in plasma, the authors report in the April 30th issue of AIDS. Her current sexual partner was tested and found to be seropositive, even though he was asymptomatic.
Dr. Cardoso’s group sequenced regions of the env and gag genes from both individuals.
Both were infected with HIV-1 subsubtype A2. That from the man had more sequence divergence, whereas that from the woman had very low genetic diversity, “consistent with a recent infection and the absence of immunologic pressure imposed on the viruses.”
“Further studies are needed to permit the identification of the immunological defect causing seronegative HIV-1 infection, because this may have important implications for diagnosis, the prevention of viral transmission and vaccination,” they conclude.
Washington Post Staff Writer
Wednesday, November 26, 2008; Page A04
A strategy of testing adults every year for HIV and immediately treating every person found to be infected could virtually end the AIDS epidemic in Africa in about a decade, new research suggests.
While nobody is seriously espousing that approach, the “thought experiment” outlined this week in the Lancet journal emphasizes the usefulness of antiretroviral drugs as tools for preventing the spread of HIV infection as well as treating it.
The power of AIDS drugs to dramatically slow the epidemic is the consequence of two well-established facts.
The first is that the amount of virus circulating in the bloodstream is the most important factor determining whether an infected person transmits the disease to another during a high-risk encounter. The second is that AIDS drugs can lower this “viral load” in the bloodstream to one-millionth of what it is without treatment.
BERLIN (Reuters) – A bone marrow transplant using stem cells from a donor with natural genetic resistance to the AIDS virus has left an HIV patient free of infection for nearly two years, German researchers.
The patient, an American living in Berlin, was infected with the human immunodeficiency virus that causes AIDS and also had leukemia. The best treatment for the leukemia was a bone marrow transplant, which takes the stem cells from a healthy donor’s immune system to replace the patient’s cancer-ridden cells.
Dr. Gero Hutter and Thomas Schneider of the Clinic for Gastroenterology, Infections and Rheumatology of the Berlin Charite hospital said on Wednesday the team sought a bone marrow donor who had a genetic mutation known to help the body resist AIDS infection.
The mutation affects a receptor, a cellular doorway, called CCR5 that the AIDS virus uses to get into the cells it infects.
When they found a donor with the mutation, they used that bone marrow to treat the patient. Not only did the leukemia disappear, but so did the HIV.
“As of today, more than 20 months after the successful transplant, no HIV can be detected in the patient,” the clinic said in a statement.
“We performed all tests, not only with blood but also with other reservoirs,” Schneider told a news conference.
“But we cannot exclude the possibility that it’s still there.”
The researchers stressed that this would never become a standard treatment for HIV. Bone marrow stem cell transplants are rigorous and dangerous and require the patient to first have his or her own bone marrow completely destroyed.
Patients risk death from even the most minor infections because they have no immune system until the stem cells can grow and replace their own.
HIV has no cure and is always fatal. Cocktails of drugs can keep the virus suppressed, sometimes to undetectable levels. But research shows the virus never disappears — it lurks in so-called reservoirs throughout the body.
Hutter’s team said they have been unable to find any trace of the virus in their 42-year-old patient, who remains unnamed, but that does not mean it is not there.
“The virus is tricky. It can always return,” Hutter said.
The CCR5 mutation is found in about 3 percent of Europeans, the researchers said. They said the study suggests that gene therapy, a highly experimental technology, might someday be used to help treat patients with HIV.
(Reporting by Oliver Denzer; Writing by Maggie Fox in Washington; Editing by Vicki Allen)
Tags: hepatitis B, hiv
[Treatment of chronic hepatitis B in HIV co-infected patients]
[Article in French]
Service d’Hepato-Gastroenterologie, Groupe hospitalier Pitie-Salpetriere, 47-83 boulevard de l’Hopital, 75651 Paris Cedex, France.
Because of complex interactions between HIV, hepatitis B virus (HBV), immune system and antiretrovirals, treatment of HBV infection in HIV population should consider both viruses. In co-infected patients with no indication of antiretrovirals, drugs with dual activity against HBV and HIV are not recommended to avoid development of HIV resistance (lamivudine, emtricitabine, entecavir, tenofovir disoproxil fumarate). Adefovir dipivoxil or pegylated interferon may be used. Telbivudine may have a role in combination with adefovir dipivoxil in this situation. In patients with an indication of antiretroviral therapy, regimens should include tenofovir in association with lamivudine or emtricitabine. In patients who had developed HBV lamivudine (or emtricitabine) resistance addition of tenofovir to antiretroviral regimen including maintenance of lamivudine or emtricitabine is the preferred choice.