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HIV Havens: Researchers Find New Clues About How HIV Reservoirs May Form
ScienceDaily (Aug. 18, 2011) — Much like cities organize contingency plans and supplies for emergencies, chronic infectious diseases like HIV form reservoirs that ensure their survival in adverse conditions. But these reservoirs -- small populations of viruses or bacteria of a specific type that persist despite attack by the immune system or drug treatment -- are not always well understood. Now, however, researchers at the California Institute of Technology (Caltech) believe they have begun to decode how a reservoir of infection can persist in HIV-positive populations.
The research team -- led by David Baltimore, Robert Andrews Millikan Professor of Biology and recipient of the 1975 Nobel Prize in Physiology or Medicine -- proposes that a type of HIV infection that uses infected cells to get close to uninfected cells and then discharge a large load of virus on them, may be the reason small populations of HIV-infected cells persist even when antiretroviral drug treatment has been successful in suppressing most other infections within an individual.
Their findings were reported in the advance online publication of the journal Nature on August 17.
For chronic infections such as HIV, the end game for scientists is to remove "chronic" from the disease's name -- by finding a cure. Many believe that better understanding of viral reservoirs may be the key to eradicating them, and thus the disease. So the research team started at the beginning of the process, looking for clues into how an HIV reservoir might be formed in the first place.
There are two known ways that HIV can infect cells, and thus the human body: cell-free transmission, in which the virus infects immune system cells called T cells it encounters while floating free in plasma; and cell-to-cell transmission, in which the virus moves between T cells by using an infected "donor" cell as its vehicle. Once an uninfected target cell is found, the donor cell can then directionally discharge its viral load upon the target. To replicate both types of transmission, the team infected target cells using both cell-free HIV and previously infected donor cells. They used donor cells that lack a natural marker, HLA-A2, usually used in matching human organ donors to recipients. The target cells did have the marker, and this helped the scientists keep track of which cells were the donors and which were the targets. The target cells were infected either in the absence or in the presence of antiretroviral drugs.
What the researchers found was that while the antiretroviral drugs caused a steep drop in the number of newly infected cells infected via cell-free transmission, the decrease in the number of newly infected cells for the cell-to-cell infected T cells was much more moderate, even when they had large doses of the drugs thrown at them.
"We saw that with cell-to-cell infection, you wind up with a lot more virus infecting a single cell," explains Alex Sigal, a postdoctoral scholar in Baltimore's laboratory and lead author of the study. "When this happens, the chance of at least a single virus getting past the drugs is much larger."
This may explain why, while antiretroviral drugs work very well, they do not eradicate the infection completely. The drugs are probabilistic by nature, meaning that they don't kill 100 percent of the virus. So, as the number of transmitted viruses gets larger, the chance of at least one virus slipping by the drugs and infecting another cell becomes greater. "And you only need one virus to infect a cell and keep the cycle going, forming a reservoir of infection," says Sigal.
Another possibility for why HIV cannot be eradicated is that it goes into latency. A latent reservoir would consist of cells that contain the HIV virus in their DNA, but are not currently making any virus and therefore are not affected by drugs. Sigal says it's possible that both types of reservoirs are present and interact with each other.
"It's important to determine whether or not cell-to-cell replication is causing a reservoir, particularly in terms of finding a cure," he says. "You can't treat it the same way as you would a latent reservoir." Theoretically, virus in a latent reservoir could be eradicated by flushing out the virus from the cells by activating it, and treating the patient with a lot of drugs at the same time so that the released virus can't enter new cells. This would not work if the virus could get into new cells anyway, despite the drugs.
"For us, the next step is to look at the process on a more physiological level by looking at how HIV infects in organs such as lymph nodes where cell-to-cell transmission actually happens," says Sigal. The team will do so by collaborating with the UCLA Center for AIDS Research, which provided the cells for virus infection from anonymous healthy volunteers in this study. The two groups will work together to increase the level of complexity in additional studies that will aim for a deeper understanding of the reservoir. "We're really looking for a cure, but to get to a cure, you have to fully understand the disease first," he says.
The Nature paper is titled "Cell-to-cell spread of HIV permits ongoing replication despite antiretroviral therapy." Jocelyn T. Kim, an infectious disease doctor and a graduate student in the Caltech-UCLA STAR Program; Alejandro B. Balazs, a postdoctoral scholar in Baltimore's laboratory; and Erez Dekel, Avi Mayo, and Ron Milo of the Weizmann Institute of Science in Israel also contributed to the study.
The research was supported by the National Institutes of Allergy and Infectious Diseases and the Bill & Melinda Gates Foundation.
The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by California Institute of Technology. The original article was written by Katie Neith.
Journal Reference:
Alex Sigal, Jocelyn T. Kim, Alejandro B. Balazs, Erez Dekel, Avi Mayo, Ron Milo, David Baltimore. Cell-to-cell spread of HIV permits ongoing replication despite
A USC scientist has created a virus that hunts down HIV-infected cells, which could herald a breakthrough toward curing the disease.
Dr. Pin Wang's lentiviral vector latches onto HIV-infected cells, flagging them with what is called "suicide gene therapy" - allowing drugs to later target and destroy them.
"If you deplete all of the HIV-infected cells, you can at least partially solve the problem," said Wang, chemical engineering professor with the USC Viterbi School of Engineering.
The lentiviral vector approach to targeting HIV has the advantage of avoiding collateral damage, keeping cells that are not infected by HIV out of harm's way.
Wang said such accuracy has not been achieved by using drugs alone.
So far, the lentiviral vector has only been tested in culture dishes and has resulted in the destruction of about 35 percent of existing HIV cells.
A USC scientist has created a virus that hunts down HIV-infected cells, which could herald a breakthrough toward curing the disease.
Dr. Pin Wang's lentiviral vector latches onto HIV-infected cells, flagging them with what is called "suicide gene therapy" - allowing drugs to later target and destroy them.
"If you deplete all of the HIV-infected cells, you can at least partially solve the problem," said Wang, chemical engineering professor with the USC Viterbi School of Engineering.
The lentiviral vector approach to targeting HIV has the advantage of avoiding collateral damage, keeping cells that are not infected by HIV out of harm's way.
Wang said such accuracy has not been achieved by using drugs alone.
So far, the lentiviral vector has only been tested in culture dishes and has resulted in the destruction of about 35 percent of existing HIV cells.
Researchers in United States reveal that they have developed a new super drug that could treat a number of diseases including HIV and should arrive in the market within the next 10 years.
According to the researchers at Massachusetts Institute of Technology, the drug, known by its acronym as DARCO, will be able to treat polio, flu, HIV, rabies, German measles, dengue fever, stomach bug and human rhinoviruses.
In the report, published in the journal PLoS One, the researchers wrote that the drug works by targeting a specific type of RNA that is produced only in cells that have been infected by a virus and said that it should be able to treat any disease that has been caused by viral infection.
Withania somnifera, also known as Ashwagandha, Indian ginseng, Winter cherry, Ajagandha, Kanaje Hindi, Amukkara in Tamil and Samm Al Ferakh, is a plant in the Solanaceae or nightshade family. Many closely related species like Withania coagulans(Dunal) – Paneer dodi, Ashutosh booti (Sanskrit, Hindi) [2] are morphologically very similar to the species.
It grows as a short shrub (35–75 cm) with a central stem from which branch extend radially in a star pattern (stellate) and covered with a dense matte of wooly hairs (tomentose).[3] The flowers are small and green, while the ripe fruit is orange-red and has milk-coagulating properties.[3] The plant also has long brown tuberous roots that are used for medicinal purposes. It is cultivated in many of the drier regions of India such as Manasa, Neemuch, and Jawad tehsils of the Mandsaur District of Madhya Pradesh, Punjab, Sind, and Rajasthan.[3]
In Ayurveda, the roots of W. somnifera are used to prepare medicinal Ashwagandha. It is claimed that Ashwaganda has been traditionally used to treat various symptoms and conditions, although there are few scientific studies of the health benefits of the compound[3][4][5][6][7][8]
The berries can be used as a substitute for rennet, to coagulate milk in cheese making.[3] The berries and leaves are traditionally used a topical treatment for tumors and tubercular glands, carbuncles and ulcers.[3][9][10]
While Ashwagandha is claimed to have a wide variety of health benefits, there have been few clinical trials to test these claims. Studies in rodents suggest that W. somnifera may reduce morphine tolerance[11][12] and to inhibit oxidative stress associated with neurologocal disorders.[13] In in vitro studies of isolated cultured cells, Ashwagandha was reported to have anti-carcinogenic effects via decreased expression of nuclear factor-kappaB, suppression of intercellular tumor necrosis factor, and potentiation of apoptotic signalling.[14]
In addition, there are registered clinical trials in progress to determine if W. somnifera is useful for treating tuberculosis,[15] Parkinsons disease[16] bone cancer,[17] bipolar disorder,[18]and diabetes,[19][20] and for improving the well-being of the elderly and breast cancer patients undergoing chemotherapy[21][22]
In at least two published clinical trials of Withania somnifera, the side effects experienced by W. somnifera treated individuals were not significantly different than the side effects experienced by placebo treated individuals. If taken in excess it can cause liver failure.[8][23] However, there has been one report that Withania somnifera can stimulate the thyroid and lead to thyrotoxicosis in some people.[24]
Ashwagandha in Sanskrit means "horse's smell," probably originating from the odor of its root which resembles that of a sweaty horse. In Tamil, it is called Amukkrang Kilangu (à®…à®®ுக்கராà®™்கிà®´à®™்கு) and is used in several medicines. The species name somnifera means "sleep-inducing" in Latin, indicating that to it are attributed sedating properties.Some herbalists refer to ashwagandha as Indian ginseng, since it is used in ayurvedic medicine in a way similar to that ginseng is used in traditional Chinese medicine.
Seven American and four Japanese firms have filed for grant of patents on formulations containing extracts of the herb Ashwagandha. It is also found in Nepal
Phytochemical investigations of multiple shoot cultures of selected accessions AGB002 and AGB025 of Withania somnifera. established in vitro utilizing shoot tip apices cultured on Murashige and Skoog's medium supplemented with BAP (1 mg/L) have been carried out. This has led to isolation of four glycowithanolides viz. Withanoside IV (WSG-3), Withanoside VI (WSG-3A), Physagulin D (WSG-P) and Withastraronolide (WSC-O).The structures of these have been confirmed on the basis of spectroscopic data. Multiple shoot cultures could be an alternative renewable resource for production of these biologically active molecules[25]
Withaferin-A (WA) is a bioactive compound derived from Withania somnifera, which inhibits Notch-1 signaling and downregulates prosurvival pathways, such as Akt/NF-κB/Bcl-2, in three colon cancer cell lines (HCT-116, SW-480, and SW-620)[26] Recent research in mice suggests that Withaferin-A may have anti-metastatic activity.[27]
Withania somnifera is prone to several pests and diseases. Leaf spot disease of Withania somnifera caused by Alternaria alternata is the most prevalent disease. It is most severe in Indian plains of Punjab, Haryana and Himachal Pradesh. Dr. Pratap Kumar Pati research group from Guru Nanak Dev University Punjab, India, recently reported in an article of Indian journal of microbiology, on the biodeterioration of its pharmacutically active components during leaf spot disease. [28] They have studied the post infectional biochemical changes and the activities of various enzymes, with the disease progression. Further, they have successfully developed a molecular detection system for the pathogen.
Grown as late rainy season (kharif) crop. The semi-tropical areas receiving 500 to 750 mm rainfall are suitable for its cultivation as rainfed crop. If one or two winter rains are received, the root development improves.
The crop requires relatively dry season during its growing period. It can tolerate a temperature range of 20 to 38 °C and even low temperature as low as 10 °C. The plant grows from sea level to an altitude of 1500 meters above sea level.
There are two sub-species of Withania somnifera - W. somnifera (ashwagandha) Kaul and W. somnifera Dunal. The sub-species Withania ashwagandha Kaul has been named after Indian botanist Kailas Nath Kaul, who was the pioneer of modern scientific research on the plant. [29] There are 23 species of the Withaniagenus that occur in the dry parts of India, North Africa, Middle East, and the Mediterranean.[3]
^ abcdefgMirjalili MH, Moyano E, Bonfill M, Cusido RM, Palazón J (2009). "Steroidal lactones from Withania somnifera, an ancient plant for novel medicine". Molecules14 (7): 2373–93. doi:10.3390/molecules14072373. PMID19633611.
^Scartezzini P, Speroni E (July 2000). "Review on some plants of Indian traditional medicine with antioxidant activity". J Ethnopharmacol71 (1-2): 23–43. doi:10.1016/S0378-8741(00)00213-0. PMID10904144.
^ Scientific basis for the use of Indian ayurvedic medicinal plants in the treatment of neurodegenerative disorders: 1. Ashwagandha Murthy M.R.V., Ranjekar P.K., Ramassamy C., Deshpande M. Central Nervous System Agents in Medicinal Chemistry 2010 10:3 (238-246)
^ Shoeb Ahmad, Abdul Hannan, S Z Rahman, Shema Wasi, Role of Withania somnifera in the management of abnormal nocturnal emission. UniMed Kulliyat Vol 2 (1) 2006: 45-4
^ Withania somnifera improves semen quality by regulating reproductive hormone levels and oxidative stress in seminal plasma of infertile malesAhmad M.K., Mahdi A.A., Shukla K.K., Islam N., Rajender S., Madhukar D., Shankhwar S.N., Ahmad S.
^ <Nadkarni, K.M. Indian Materia Medica; Popular Prakshan Limited: Bombay, India, 1976; p. 1291.
^L. D. Kapoor (2001). Handbook of Ayurvedic medicinal plants. Boca Raton: CRC Press. ISBN0-8493-2929-9.
^Lu L, Liu Y, Zhu W, et al. (2009). "Traditional medicine in the treatment of drug addiction". Am J Drug Alcohol Abuse35 (1): 1–11. doi:10.1080/00952990802455469. PMID19152199.
^ Withania somnifera prevents morphine withdrawal-induced decrease in spine density in nucleus accumbens shell of rats: A confocal laser scanning microscopy studyKasture S., Vinci S., Ibba F., Puddu A., Marongiu M., Murali B., Pisanu A., Lecca D., Zernig G., Acquas E. Neurotoxicity Research 2009 16:4 (343-355)
^ Neuroprotective effects of withania somnifera dunal.: A possible mechanism Bhatnagar M., Sharma D., Salvi M. Neurochemical Research 2009 34:11 (1975-1983)
^Ichikawa H, Takada Y, Shishodia S, Jayaprakasam B, Nair MG, Aggarwal BB (June 2006). "Withanolides potentiate apoptosis, inhibit invasion, and abolish osteoclastogenesis through suppression of nuclear factor-kappaB (NF-kappaB) activation and NF-kappaB-regulated gene expression". Molecular Cancer Therapeutics5 (6): 1434–45. doi:10.1158/1535-7163.MCT-06-0096. PMID16818501.
^Chopra A, Lavin P, Patwardhan B, Chitre D (October 2004). "A 32-week randomized, placebo-controlled clinical evaluation of RA-11, an Ayurvedic drug, on osteoarthritis of the knees". J Clin Rheumatol10 (5): 236–45. doi:10.1097/01.rhu.0000138087.47382.6d. PMID17043520.
^van der Hooft CS, Hoekstra A, Winter A, de Smet PA, Stricker BH (November 2005). "[Thyrotoxicosis following the use of ashwagandha]" (in Dutch). Nederlands Tijdschrift Voor Geneeskunde149 (47): 2637–8. PMID16355578.
^ Glycowithanolides accumulation in in vitro shoot cultures of Indian ginseng (Withania somnifera dunal)Ahuja A., Kaur D., Sharada M., Kumar A., Suri K.A., Dutt P. Natural Product Communications 2009 4:4 (479-482)
^Koduru S., Kumar R., Srinivasan S., Evers M.B., Damodaran C. (2010). 9. Molecular Cancer Therapeutics. pp. 202–210. Notch-1 inhibition by withaferin-A: A therapeutic target against colon carcinogenesis.
^Thaiparambil, JT.; Bender, L.; Ganesh, T.; Kline, E.; Patel, P.; Liu, Y.; Tighiouart, M.; Vertino, PM. et al. (Jan 2011). "Withaferin A inhibits breast cancer invasion and metastasis at sub-cytotoxic doses by inducing vimentin disassembly and serine 56 phosphorylation.". Int J Cancer. doi:10.1002/ijc.25938. PMID21538350.
^ Kaul K. N. 1956. The origin, distribution and cultivation of Ashwangandha, the so called Withania somnifera of Indian literature. Symposium on the utilisation of Indian Medicinal Plants; Lucknow CSIR.pp.07-08
Long ago - before the births of Buddhism, Yoga and Christianity - there was historical record of the uses of Aswagandha as a healing herb in India. Today, after thousands of years of continuous use, still Aswagandha is regarded as one of the most valuable Ayurvedic medicinal plants. Botanical name – Withania somnifera Family – Solanaceae
Synonyms
Sanskrit : Hayagandha, Vajigandh
Assamese : Ashvagandha
Bengali : Ashvagandha
English : Winter Cherry
Gujrati : Asgandha
Hindi : Asgandh
Kannada : Angarberu, Hiremaddina-gida
Kashmiri : Asagandh
Malayalam : Amukkuram
Marathi : Asagandha, Askagandha
Oriya : Aswagandha
Punjabi : Asgandh
Tamil : Amukkaramkizangu
Telugu : Pennerugadda
Urdu : Asgand
Geographical distribution
It is a short shrub grows in all dry parts and sub tropical parts of India such as Punjab, Madhya Pradesh, Gujarat, and Rajasthan. It is also found in South Africa, Congo, Egypt, Morocco, Jordan and Afghanistan.
Plant Facts :
It is a short shrub (35-75 cm) with a central stem from which branch extend radially like a star and covered with a dense matte of wooly hairs. The plant also has long brown tuberous roots that are used for medicinal purposes. Parts Used - Dried Roots and Stem base
All chemicals listed pertain to the root unless otherwise specified, as the root is the part used. Anaferine (alkaloid), anahygrine (alkaloid), beta-sisterol, chlorogenic acid (in leaf only), cysteine (in fruit), cuscohygrine (alkaloid), iron, pseudotropine (alkaloid), scopoletin, somniferinine (alkaloid), somniferiene (alkaloid), tropanol (alkaloid), withaferin A (steroidal lactone), withanine (alkaloid), withananine (alkaloid) and withanolides A-Y(steroidal lactones). The main constituents of Aswagandha are alkaloids and steroidal lactones. Among the various alkaloids, withanine is the main constituent. The other alkaloids are somniferine, somnine, somniferinine, withananine, pseudo-withanine, tropine, pseudo-tropine, 3-a-gloyloxytropane, choline, cuscohygrine, isopelletierine, anaferine and anahydrine. Two acyl steryl glucoside viz. sitoindoside VII and sitoindoside VIII have been isolated from root. The leaves contain steroidal lactones, which are commonly called withanolides. The withanolides have C28 steroidal nucleus with C9 side chain, having six membered lactone rings.
"The Queen of Herbs" - is the most sacred herb of India. Tulsi (Ocimum sanctum), although also known as Holy Basil, is a different plant from the pesto variety of Basil (Ocimum basilicum). Tulsi has been revered in India for over five thousand years, as a healing balm for body, mind and spirit, and is known to bestow an amazing number of health benefits. ORGANIC INDIA is pleased to offer Organic Tulsi, for the first time, as a stress-relieving, energizing and delicious tea. For our ORGANIC INDIA Tulsi Tea Collection we utilize a proprietary combination of 3 varieties of Tulsi: Rama Tulsi (Ocimum sanctum), Krishna Tulsi (Ocimum sanctum) and Vana Tulsi (Ocimum gratissimum). Each variety lends its own distinct and characteristic taste that contributes to the delicious flavor and aroma of our blend.
What are the health benefits of Tulsi?
Tulsi is rich in antioxidant and renowned for its restorative powers, Tulsi has several benefits:
Relieves stress / adaptogen
Bolsters immunity
Enhances stamina
Provides support during cold season
Promotes healthy metabolism
A natural immuno-modulator
"Modern scientific research offers impressive evidence that Tulsi reduces stress, enhances stamina, relieves inflammation, lowers cholesterol, eliminates toxins, protects against radiation, prevents gastric ulcers, lowers fevers, improves digestion and provides a rich supply of antioxidants and other nutrients. Tulsi is especially effective in supporting the heart, blood vessels, liver and lungs and also regulates blood pressure and blood sugar." Dr. Ralph Miller, former Director of Research for the Canadian Dept. of Health and Welfare.
How can Tulsi offer so many health benefits?
The unique chemistry of Tulsi is highly complex. Tulsi contains hundreds of beneficial compounds known as phyto-chemicals. Working together, these compounds possess strong antioxidant, antibacterial, antiviral, adaptogenic, and immune-enhancing properties that promote general health and support the body's natural defense against stress and diseases. The essential oils in the leaves of Tulsi that contribute to the fragrance and refreshing flavor of Tulsi Tea, are a particularly rich source of valuable phyto-chemicals.
What is an adaptogen?
An adaptogen is an agent that helps the body adapt more efficiently to stress. Adaptogens reduce the intensity and negative impact of the stress caused by mental tension, emotional difficulties, poor lifestyle habits, disease and infection, pollution and other factors. Tulsi is one of the most effective adaptogens known.
What are antioxidants?
Antioxidants slow down the process of excess oxidation and protect cells from the damage caused by free radicals. When cells are attacked by free radicals, excess oxidation occurs which damage and destroy cells. Antioxidants stop this process. The cellular damage caused by free radicals can be responsible for causing and/or accelerating many diseases. Tulsi is rich in antioxidants and is recommended to guard against free radicals and protect from damaging excess oxidation.
What is an immuno-modulator?
An immuno-modulator is an agent that balances and improves the immune response of the body in fighting antigens (disease causing agents such as bacteria, viruses, microbes, allergens etc.) and maintaining health.
How soon can I expect to see results from drinking ORGANIC INDIA Tulsi Teas?
Some of Tulsi effects are quite immediate, while others develop gradually after weeks of regular use. For example, you may feel more relaxed and energized after the first cup. Although Tulsi has many specific effects on different body systems, its main benefits arise from its impressive general capacity to assist the body's natural process of healing and maintaining health. Tulsi overall health promotion and disease prevention effects are powerful, but often subtle. For example, you may simply notice that you do not seem to be bothered by stress or common illnesses, such as colds or flu, nearly as often as before. Or you may notice that you generally tire less easily. As with many other herbal supplements, it usually takes at least a week or so of consistent use for the body to experience major benefits.
