We accomplished this by using a gene encoding an RNA replicase polyprotein derived from the Semliki forest virus, in combination with a model antigen. Pre-immunization with a self-replicating RNA vector protected mice from tumor challenge, and therapeutic immunization prolonged the survival of mice with established tumors.
Smith July Bruce T. By using more than one drug at a time, combination therapy is able to "pin down" HIV from more than one angle, so that even if one drug fails, another can continue to suppress viral replication.
But this advance was a long time in the making, following a historical course from "no therapy" to "monotherapy" and now to "combination therapy.
Although medical progress has often seemed slow in coming, advances in knowledge about AIDS have in many ways actually been swift.
Within a year, epidemiological evidence had made clear that the causative agent of AIDS was sexually transmissible, and that it had particularly spread within sexual networks of gay men. Advertisement Further research gradually determined the precise means by which HIV invades the human body.
After entering a cell of the immune system, the virus begins a relentless process of replication, its sole activity and one which allows for a constant spread to new cells.
In the process, the immune system of the host organism can be devastated. The virus's outer coat consists of particular glycoproteins, which can form biochemical bonds with particular proteins such as CD4 that are found on the surface of some cells, notably those in the immune system.
Once bonding occurs, the HIV life cycle requires the insertion of its own genetic material into the host cell and ultimately the use of three important viral enzymes. The third, protease, later cleaves off new copies of the viral proteins, allowing new virus particles to be assembled and enabling these new viruses to leave the cell.
These three enzymes are essential to the process of viral replication, and most advances in HIV treatment have come from inhibiting the activity of these enzymes. AZT is part of a class of drugs formally known as nucleoside analog reverse transcriptase inhibitors.
Afterseveral other nucleoside analogs were added to the anti-HIV arsenal, as were a new class of anti-HIV drugs called the non-nucleoside analog reverse transcriptase inhibitors which work in similar ways to the nucleoside analogs but which are more quickly activated once inside the bloodstream.
Next to be developed were the class of antiviral drugs known as protease inhibitors, which were distinctly different from the reverse transcriptase inhibitors in that they do not seek to prevent infection of a host cell, but rather to prevent an already infected cell from producing more copies of HIV.
Despite this proliferation of drug options, the standard antiviral therapy for HIV-infected individuals between and for the most part remained "monotherapy" or treatment with a single drug. Such drugs appeared to be partly efficacious, although there was a great variation in effectiveness among individuals.
During this period, there were also significant advances in the understanding of how HIV functions in the body. In particular, whereas it was once believed that individuals went into a latency period of ten years or more after their initial infection with HIV, it came to be understood that huge amounts of viral replication continued throughout the entire period of infection, even if an individual was not exhibiting any symptoms of illness.
Thus, the onset of symptoms of AIDS is now known to be the result not of a sudden resurgence of a latent virus, but rather of a slow "war of attrition" between HIV and the host immune system, with the latter slowly being whittled away by the former. The recognition of the persistence of viral replication -- with billions of copies of HIV being produced and destroyed daily -- also made possible a better understanding of the process by which the virus gradually becomes less sensitive to specific antiviral medications, a process known as developing resistance.
Such resistance generally occurs when a random mutation during the replication of HIV causes a small genetic change in the virus's RNA, in the process making it less vulnerable to the effects of antiviral drugs. Drug resistance can seriously complicate treatment by rendering drugs less effective or even completely ineffective.
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Further, once an organism has developed resistance to one drug, it can also become resistant to other drugs in the same class cross-resistance or to a number of different drugs multidrug resistance. From this perspective, it could be seen that monotherapy against HIV was of limited usefulness because HIV could quickly develop resistance to any one medication.
However, the expansion of the number of distinct classes of antiviral medications made possible a shift from monotherapy to combination therapy, in which drugs from two or more classes are used simultaneously.
This switch to combination therapy has had dramatic effects because "in essence, combination therapy suffocates mutated forms of HIV before they have a chance to flourish. For example, in a combination of ddId4Tand indinavira strain of HIV that is naturally resistant to ddI will be kept in check by d4T and indinavir, while a strain of HIV that is resistant to indinavir will be kept in check by d4T and ddI" Horn When nucleoside analog drugs, the non-nucleoside analog drugs, and the protease inhibitors are used in concert, these drug combinations are referred to as " highly active antiretroviral therapy " or HAART.
By the start ofcombination therapy had become the standard of care for HIV-infected individuals who have begun to exhibit signs of significant immunosuppression, although no clear cut consensus has emerged about the best time to initiate therapy.
This decision must be based on balancing a variety of factors including the length of time since initial infection, current CD4 cell count and viral loadclinical prognosis, side effect profile, and the individual's psychological readiness and motivation to begin and adhere to treatment.Database of research protocols in bioscience including molecular biology, cell biology, immunology, plant biology, developmental biology, neuroscience, bioinformatics, genetics, etc.
Also hosts discipline-specific discussion forums and provides free PubMed alerting service. DNA computing: DNA computing, the performing of computations using biological molecules, rather than traditional silicon chips.
The idea that individual molecules (or even atoms) could be used for computation dates to , when American physicist Richard Feynman presented his ideas on nanotechnology. However.
DNA's chemical properties can be harnessed for a variety of biotechnology applications. Learn the principles of how DNA is sequenced and assembled into whole genomes using the Sanger method, shotgun sequencing, or ultra-deep sequencing.
Answer interactive questions to explore the logic of the. Genetics Real-Time PCR Homepage. GLOSSARY OF REAL-TIME PCR TERMS. alphabetnyc.com Dorak. Address for bookmark: alphabetnyc.com Absolute.
A new method for replicating DNA in the lab, named COMPAS-PCR, short for COMplementary Primer Asymmetric PCR, has been developed by scientists at the Norwegian Institute for Water Research.
Analyzing DNA is useful for a number of vital applications. This includes diagnosis and monitoring of diseases, identification of . What will a Southern blot of the same gene look like after PCR?
A) a B) b C) c D) d E) e. Self-replicating DNA used to transmit a gene from one organism to another is a A) Library. B) Clone. Which of the following processes CANNOT be used to insert foreign DNA into cells? A) Transformation B) Electroporation.