Research that attempts to reproduce the findings of previous investigators so as to increase confidence in (or refute) those findings.
Both HIV-1 and HIV-2 are predominantly sexually transmitted and both are associated with secondary opportunistic infections. However, HIV-2 seems to result in slower damage to the immune system. HIV-1 is known to mutate rapidly and has given rise to other subtypes.
HIV is thought to have occurred in humans in the 1950s, but whether or not it infected humans from another primate species is uncertain. It became widespread in the 1970s but its latency in causing symptoms meant that the epidemic was not noticed until the following decade. Although it is a sexually transmitted disease, it can also be transmitted by intravenous drug use (through sharing an infected needle), blood transfusions with infected blood (hence the importance of e?ective national blood-screening programmes), organ donation, and occupationally (see health-care workers, below). Babies born of HIV-positive mothers can be infected before or during birth, or through breast feeding.
Although HIV is most likely to occur in blood, semen or vaginal ?uid, it has been found in saliva and tears (but not sweat); however, there is no evidence that the virus can be transmitted from these two body ?uids. There is also no evidence that HIV can be transmitted by biting insects (such as mosquitoes). HIV does not survive well in the environment and is rapidly destroyed through drying.
Prevalence At the end of 2003 an estimated 42 million people globally were infected with HIV – up from 40 million two years earlier. About one-third of those with HIV/AIDS are aged 15–24 and most are unaware that they are carrying the virus. During 2003 it is estimated that 5 million adults and children worldwide were newly infected with HIV, and that 3 million adults and children died. In Africa in 2003,
3.4 million people were newly infected and 2.3 million died, with more than 28 million carrying the virus. HIV/AIDS was the leading cause of death in sub-Saharan Africa where over half of the infections were in women and 90 per cent of cases resulted from heterosexual sex. In some southern African countries, one in three pregnant women had HIV.
In Asia and the Paci?c there were 1.2 million new infections and 435,000 deaths. The area with the fastest-growing epidemic is Eastern Europe, especially the Russian Federation where in 2002 around a million people had HIV and there were an estimated 250,000 new infections, with intravenous drug use a key contributor to this ?gure. Seventy-?ve per cent of cases occurred in men, with male-to-male sexual transmission an important cause of infection, though heterosexual activity is a rising cause of infection.
At the end of 2002 the UK had an estimated 55,900 HIV-infected adults aged between 15 and 59. More than 3,600 individuals were newly diagnosed with the infection in 2000, the highest annual ?gure since the epidemic started
– in 1998 the ?gure was 2,817 and in 1999 just over 3,000 (Department of Health and Communicable Disease Surveillance Centre). The incidence of AIDS in the UK has declined sharply since the introduction of highly active antiretroviral therapy (HAART) and HIV-related deaths have also fallen: in 2002 there were 777 reported new AIDS cases and 395 deaths, compared with 1,769 and 1,719 respectively in 1995. (Sources: UNAIDS and WHO, AIDS Epidemic Update, December 2001; Public Health Laboratory Services AIDS and STD Centre Communicable Disease Surveillance and Scottish Centre for Infection and Environmental Health, Quarterly Surveillance Tables.)
Poverty is strongly linked to the spread of AIDS, for various reasons including lack of health education; lack of e?ective public-health awareness; women having little control over sexual behaviour and contraception; and, by comparison with the developed world, little or no access to antiretroviral drugs.
Pathogenesis The cellular target of HIV infection is a subset of white blood cells called T-lymphocytes (see LYMPHOCYTE) which carry the CD4 surface receptor. These so-called ‘helper T-cells’ are vital to the function of cell-mediated immunity. Infection of these cells leads to their destruction (HIV replicates at an enormous rate – 109) and over the course of several years the body is unable to generate suf?cient new cells to keep pace. This leads to progressive destruction of the body’s immune capabilities, evidenced clinically by the development of opportunistic infection and unusual tumours.
Monitoring of clinical progression It is possible to measure the number of viral particles present in the plasma. This gives an accurate guide to the likely progression rate, which will be slow in those individuals with fewer than 10,000 particles per ml of plasma but progressively more rapid above this ?gure. The main clinical monitoring of the immune system is through the numbers of CD4 lymphocytes in the blood. The normal count is around 850 cells per ml and, without treatment, eventual progression to AIDS is likely in those individuals whose CD4 count falls below 500 per ml. Opportunistic infections occur most frequently when the count falls below 200 per ml: most such infections are treatable, and death is only likely when the CD4 count falls below 50 cells per ml when infection is developed with organisms that are di?cult to treat because of their low intrinsic virulence.
Simple, cheap and highly accurate tests are available to detect HIV antibodies in the serum. These normally occur within three months of infection and remain the cornerstone of the diagnosis.
Clinical features Most infected individuals have a viral illness some three weeks after contact with HIV. The clinical features are often non-speci?c and remain undiagnosed but include a ?ne red rash, large lymph nodes, an in?uenza-like illness, cerebral involvement and sometimes the development of opportunistic infections. The antibody test may be negative at this stage but there are usually high levels of virus particles in the blood. The antibody test is virtually always positive within three months of infection. HIV infection is often subsequently asymptomatic for a period of ten years or more, although in most patients progressive immune destruction is occurring during this time and a variety of minor opportunistic infections such as HERPES ZOSTER or oral thrush (see CANDIDA) do occur. In addition, generalised LYMPHADENOPATHY is present in a third of patients and some suffer from severe malaise, weight loss, night sweats, mild fever, ANAEMIA or easy bruising due to THROMBOCYTOPENIA.
The presentation of opportunistic infection is highly variable but usually involves either the CENTRAL NERVOUS SYSTEM, the gastrointestinal tract or the LUNGS. Patients may present with a sudden onset of a neurological de?cit or EPILEPSY due to a sudden onset of a STROKE-like syndrome, or epilepsy due to a space-occupying lesion in the brain – most commonly TOXOPLASMOSIS. In late disease, HIV infection of the central nervous system itself may produce progressive memory loss, impaired concentration and mental slowness called AIDS DEMENTIA. A wide variety of opportunistic PROTOZOA or viruses produces DYSPHAGIA, DIARRHOEA and wasting. In the respiratory system the commonest opportunistic infection associated with AIDS, pneumonia, produces severe shortness of breath and sometimes CYANOSIS, usually with a striking lack of clinical signs in the chest.
In very late HIV infection, when the CD4 count has fallen below 50 cells per ml, infection with CYTOMEGALOVIRUS may produce progressive retinal necrosis (see EYE, DISORDERS OF) which will lead to blindness if untreated, as well as a variety of gastrointestinal symptoms. At this stage, infection with atypical mycobacteria is also common, producing severe anaemia, wasting and fevers. The commonest tumour associated with HIV is Kaposi’s sarcoma which produces purplish skin lesions. This and nonHodgkin’s lymphoma (see LYMPHOMA), which is a hundred times more frequent among HIV-positive individuals than in the general population, are likely to be associated with or caused by opportunistic viral infections.
Prevention There is, as yet, no vaccine to prevent HIV infection. Vaccine development has been hampered
by the large number of new HIV strains generated through frequent mutation and recombination.
because HIV can be transmitted as free virus and in infected cells.
because HIV infects helper T-cells – the very cells involved in the immune response. There are, however, numerous research pro
grammes underway to develop vaccines that are either prophylactic or therapeutic. Vaccine-development strategies have included: recombinant-vector vaccines, in which a live bacterium or virus is genetically modi?ed to carry one or more of the HIV genes; subunit vaccines, consisting of small regions of the HIV genome designed to induce an immune response without infection; modi?ed live HIV, which has had its disease-promoting genes removed; and DNA vaccines – small loops of DNA (plasmids) containing viral genes – that make the host cells produce non-infectious viral proteins which, in turn, trigger an immune response and prime the immune system against future infection with real virus.
In the absence of an e?ective vaccine, preventing exposure remains the chief strategy in reducing the spread of HIV. Used properly, condoms are an extremely e?ective method of preventing exposure to HIV during sexual intercourse and remain the most important public-health approach to countering the further acceleration of the AIDS epidemic. The spermicide nonoxynol-9, which is often included with condoms, is known to kill HIV in vitro; however, its e?ectiveness in preventing HIV infection during intercourse is not known.
Public-health strategies must be focused on avoiding high-risk behaviour and, particularly in developing countries, empowering women to have more control over their lives, both economically and socially. In many of the poorer regions of the world, women are economically dependent on men and refusing sex, or insisting on condom use, even when they know their partners are HIV positive, is not a straightforward option. Poverty also forces many women into the sex industry where they are at greater risk of infection.
Cultural problems in gaining acceptance for universal condom-use by men in some developing countries suggests that other preventive strategies should also be considered. Microbicides used as vaginal sprays or ‘chemical condoms’ have the potential to give women more direct control over their exposure risk, and research is underway to develop suitable products.
Epidemiological studies suggest that male circumcision may o?er some protection against HIV infection, although more research is needed before this can be an established public-health strategy. Globally, about 70 per cent of infected men have acquired the virus through unprotected vaginal sex; in these men, infection is likely to have occurred through the penis with the mucosal epithelia of the inner surface of the foreskin and the frenulum considered the most likely sites for infection. It is suggested that in circumcised men, the glans may become keratinised and thus less likely to facilitate infection. Circumcision may also reduce the risk of lesions caused by other sexually transmitted disease.
Treatment AIDS/HIV treatment can be categorised as speci?c therapies for the individual opportunistic infections – which ultimately cause death – and highly active antiretroviral therapy (HAART) designed to reduce viral load and replication. HAART is also the most e?ective way of preventing opportunistic infections, and has had a signi?cant impact in delaying the onset of AIDS in HIV-positive individuals in developed countries.
Four classes of drugs are currently in use. Nucleoside analogues, including ZIDOVUDINE and DIDANOSINE, interfere with the activity of the unique enzyme of the retrovirus reverse transcriptase which is essential for replication. Nucleotide analogues, such as tenofovir, act in the same way but require no intracellular activation. Non-nucleoside reverse transcriptase inhibitors, such as nevirapine and EFAVIRENZ, act by a di?erent mechanism on the same enzyme. The most potent single agents against HIV are the protease inhibitors, such as lopinavir, which render a unique viral enzyme ineffective. These drugs are used in a variety of combinations in an attempt to reduce the plasma HIV viral load to below detectable limits, which is achieved in approximately 90 per cent of patients who have not previously received therapy. This usually also produces a profound rise in CD4 count. It is likely, however, that such treatments need to be lifelong – and since they are associated with toxicities, long-term adherence is di?cult. Thus the optimum time for treatment intervention remains controversial, with some clinicians believing that this should be governed by the viral load rising above 10,000 copies, and others that it should primarily be designed to prevent the development of opportunistic infections – thus, that initiation of therapy should be guided more by the CD4 count.
It should be noted that the drug regimens have been devised for infection with HIV-1; it is not known how e?ective they are at treating infection with HIV-2.
HIV and pregnancy An HIV-positive woman can transmit the virus to her fetus, with the risk of infection being particularly high during parturition; however, the risk of perinatal HIV transmission can be reduced by antiviral drug therapy. In the UK, HIV testing is available to all women as part of antenatal care. The bene?ts of antenatal HIV testing in countries where antiviral drugs are not available are questionable. An HIV-positive woman might be advised not to breast feed because of the risks of transmitting HIV via breastmilk, but there may be a greater risk associated with not breast feeding at all. Babies in many poor communities are thought to be at high risk of infectious diseases and malnutrition if they are not breast fed and may thus be at greater overall risk of death during infancy.
Counselling Con?dential counselling is an essential part of AIDS management, both in terms of supporting the psychological wellbeing of the individual and in dealing with issues such as family relations, sexual partners and implications for employment (e.g. for health-care workers). Counsellors must be particularly sensitive to culture and lifestyle issues. Counselling is essential both before an HIV test is taken and when the results are revealed.
Health-care workers Health-care workers may be at risk of occupational exposure to HIV, either through undertaking invasive procedures or through accidental exposure to infected blood from a contaminated needle (needlestick injury). Needlestick injuries are frequent in health care – as many as 600,000 to 800,000 are thought to occur annually in the United States. Transmission is much more likely where the worker has been exposed to HIV through a needlestick injury or deep cut with a contaminated instrument than through exposure of mucous membranes to contaminated blood or body ?uids. However, even where exposure occurs through a needlestick injury, the risk of seroconversion is much lower than with a similar exposure to hepatitis C or hepatitis B. A percutaneous exposure to HIV-infected blood in a health-care setting is thought to carry a risk of about one infection per 300 injuries (one in 1,000 for mucous-membrane exposure), compared with one in 30 for hepatitis C, and one in three for hepatitis B (when the source patient is e-antigen positive).
In the event of an injury, health-care workers are advised to report the incident immediately where, depending on a risk assessment, they may be o?ered post-exposure prophylaxis (PEP). They should also wash the contaminated area with soap and water (but without scrubbing) and, if appropriate, encourage bleeding at the site of injury. PEP, using a combination of antiretroviral drugs (in a similar regimen to HAART – see above), is thought to greatly reduce the chances of seroconversion; it should be commenced as soon as possible, preferably within one or two hours of the injury. Although PEP is available, safe systems of work are considered to o?er the greatest protection. Double-gloving (latex gloves remove much of the blood from the surface of the needle during a needlestick), correct use of sharps containers (for used needles and instruments), avoiding the resheathing of used needles, reduction in the number of blood samples taken from a patient, safer-needle devices (such as needles that self-blunt after use) and needleless drug administration are all thought to reduce the risk of exposure to HIV and other blood-borne viruses. Although there have been numerous cases of health-care workers developing HIV through occupational exposure, there is little evidence of health-care workers passing HIV to their patients through normal medical procedures.... aids/hiv
Alkylating agents are important because they interfere with the growth and reproduction of cells, disrupting their replication. This CYTOTOXIC property is used to retard the division and growth of cancer cells, and alkylating drugs are widely used in the chemotherapy of malignant tumours – often in conjunction with surgery and sometimes with radiotherapy. Unfortunately, troublesome side-effects occur, such as: damage to veins when the drug is given intravenously, with resultant leakage into adjacent tissues; impaired kidney function due to the formation of URIC ACID crystals; nausea and vomiting; ALOPECIA (hair loss); suppression of BONE MARROW activity (production of blood cells); and adverse effects on reproductive function, including TERATOGENESIS. Indeed, cytotoxic drugs must not be given in pregnancy, especially during the ?rst three months. Prolonged use of alkylating drugs, especially when accompanying radiotherapy, is also associated with a sign?cant rise in the incidence of acute non-lymphocytic LEUKAEMIA. Among the dozen or so alkylating drugs in use are CYCLOPHOSPHAMIDE, CHLORAMBUCIL, MELPHALAN, BUSULFAN and THIOTEPA. (See also CHEMOTHERAPY.)... alkylating agents
Carried out as two separate exercises – one by a privately funded American team; another by an international joint venture between tax-funded American laboratories, a charitably funded British one and several other smaller research teams from around the world – the ?rst results were announced on 26 June 2000. In February 2001 the privately funded American group, known as Celera Genomics, announced that it had identi?ed 26,558 genes. At the same time the Human Genome Project consortium reported that it had identi?ed 31,000. Allowing for margins of error, this gives a ?gure much lower than the 100,000 or more human genes previously forecast by scientists. Interestingly, genes were found to make up only 3 per cent of the human genome. The remaining 97 per cent of the genome comprises non-coding DNA which, though not involved in producing the protein-initiating genetic activity, does have signi?cant roles in the structure, function and evolution of the genome.
One surprise from the Project so far is that the genetic di?erences between humans and other species seem much smaller than previously expected. For example, the Celera team found that people have only 300 genes that mice do not have; yet, the common ancestor of mice and men probably lived 100 million years or more in the past. Mice and humans, however, have around twice as many genes as the humble fruit ?y.
Cells die out when they become redundant during embryonic development: genes also die out during evolution, according to evidence from the Genome Project – a ?nding that supports the constant evolutionary changes apparent in living things; the Darwinian concept of survival of the ?ttest.
Apart from expanding our scienti?c knowledge, the new information – and promise of much more as the Genome Project continues – should enhance and expand the use of genetic engineering in the prevention and cure of disease. Studies are in progress on the gene for a receptor protein in the brain which will shed light on how the important neurotransmitter SEROTONIN in the brain works, and this, for example, should help the development of better drugs for the treatment of DEPRESSION. Another gene has been found that is relevant to the development of ASTHMA and yet another that is involved in the production of amyloid, a complex protein which is deposited in excessive amounts in both DOWN’S (DOWN) SYNDROME and ALZHEIMER’S DISEASE.... human genome
A number of plant medicines inhibit HIV-1 replication including, Turmeric, Siberian Ginseng and Garlic. ... hiv
Among the smallest and simplest microorganisms are the viruses. First described as ?lterable agents, and ranging in size from 20–30 nm to 300 nm, they may be directly visualised only by electron microscopy. They consist of a core of deoxyribonucleic or ribonucleic acid (DNA or RNA) within a protective protein coat, or capsid, whose subunits confer a geometric symmetry. Thus viruses are usually cubical (icosahedral) or helical; the larger viruses (pox-, herpes-, myxo-viruses) may also have an outer envelope. Their minimal structure dictates that viruses are all obligate parasites, relying on living cells to provide essential components for their replication. Apart from animal and plant cells, viruses may infect and replicate in bacteria (bacteriophages) or fungi (mycophages), which are damaged in the process.
Bacteria are larger (0·01–5,000 µm) and more complex. They have a subcellular organisation which generally includes DNA and RNA, a cell membrane, organelles such as ribosomes, and a complex and chemically variable cell envelope – but, unlike EUKARYOTES, no nucleus. Rickettsiae, chlamydia, and mycoplasmas, once thought of as viruses because of their small size and absence of a cell wall (mycoplasma) or major wall component (chlamydia), are now acknowledged as bacteria; rickettsiae and chlamydia are intracellular parasites of medical importance. Bacteria may also possess additional surface structures, such as capsules and organs of locomotion (?agella) and attachment (?mbriae and stalks). Individual bacterial cells may be spheres (cocci); straight (bacilli), curved (vibrio), or ?exuous (spirilla) rods; or oval cells (coccobacilli). On examination by light microscopy, bacteria may be visible in characteristic con?gurations (as pairs of cocci [diplococci], or chains [streptococci], or clusters); actinomycete bacteria grow as ?laments with externally produced spores. Bacteria grow essentially by increasing in cell size and dividing by ?ssion, a process which in ideal laboratory conditions some bacteria may achieve about once every 20 minutes. Under natural conditions, growth is usually much slower.
Eukaryotic micro-organisms comprise fungi, algae, and protozoa. These organisms are larger, and they have in common a well-developed internal compartmentation into subcellular organelles; they also have a nucleus. Algae additionally have chloroplasts, which contain photosynthetic pigments; fungi lack chloroplasts; and protozoa lack both a cell wall and chloroplasts but may have a contractile vacuole to regulate water uptake and, in some, structures for capturing and ingesting food. Fungi grow either as discrete cells (yeasts), multiplying by budding, ?ssion, or conjugation, or as thin ?laments (hyphae) which bear spores, although some may show both morphological forms during their life-cycle. Algae and protozoa generally grow as individual cells or colonies of individuals and multiply by ?ssion.
Micro-organisms of medical importance include representatives of the ?ve major microbial groups that obtain their essential nutrients at the expense of their hosts. Many bacteria and most fungi, however, are saprophytes (see SAPROPHYTE), being major contributors to the natural cycling of carbon in the environment and to biodeterioration; others are of ecological and economic importance because of the diseases they cause in agricultural or horticultural crops or because of their bene?cial relationships with higher organisms. Additionally, they may be of industrial or biotechnological importance. Fungal diseases of humans tend to be most important in tropical environments and in immuno-compromised subjects.
Pathogenic (that is, disease-causing) microorganisms have special characteristics, or virulence factors, that enable them to colonise their hosts and overcome or evade physical, biochemical, and immunological host defences. For example, the presence of capsules, as in the bacteria that cause anthrax (Bacillus anthracis), one form of pneumonia (Streptococcus pneumoniae), scarlet fever (S. pyogenes), bacterial meningitis (Neisseria meningitidis, Haemophilus in?uenzae) is directly related to the ability to cause disease because of their antiphagocytic properties. Fimbriae are related to virulence, enabling tissue attachment – for example, in gonorrhoea (N. gonorrhoeae) and cholera (Vibrio cholerae). Many bacteria excrete extracellular virulence factors; these include enzymes and other agents that impair the host’s physiological and immunological functions. Some bacteria produce powerful toxins (excreted exotoxins or endogenous endotoxins), which may cause local tissue destruction and allow colonisation by the pathogen or whose speci?c action may explain the disease mechanism. In Staphylococcus aureus, exfoliative toxin produces the staphylococcal scalded-skin syndrome, TSS toxin-1 toxic-shock syndrome, and enterotoxin food poisoning. The pertussis exotoxin of Bordetella pertussis, the cause of whooping cough, blocks immunological defences and mediates attachment to tracheal cells, and the exotoxin produced by Corynebacterium diphtheriae causes local damage resulting in a pronounced exudate in the trachea.
Viruses cause disease by cellular destruction arising from their intracellular parasitic existence. Attachment to particular cells is often mediated by speci?c viral surface proteins; mechanisms for evading immunological defences include latency, change in viral antigenic structure, or incapacitation of the immune system – for example, destruction of CD 4 lymphocytes by the human immunode?ciency virus.... microbiology
Habitat: Native to Sri Lanka; grown in gardens throughout the warmer parts of India.
English: Mast tree, Fake Asoka tree, False Devadaru, Cemetry treeAyurvedic: Devadaari (Devadaaru is equated with Cedrus deodara). (An adulterant to the bark of Saraca asoca.)Siddha/Tamil: Nettilingam.Action: Febrifuge. Causes cardiac depression.
The stem bark contains clerodane diterpenes, polyalthialdoic acid and kolavenic acid. The stem and its bark also contain the cytotoxic aporphine alkaloid, liriodenine, besides nor-oli- veroline and oliveroline-beta-N-oxide. Azafluorene alkaloids are also present in the bark and leaves. The leaf exhibits fungitoxic activity.Polyalthia simiarum Hook. f. & Thoms. (Orissa, Assam, Bengal, Bihar, Eastern Himalaya) is also equated with Fake Ashoka tree. It is known as Boga-khamtou in Assam, Wojarah, Mongai in Orissa and Labshi, Kutti in Nepal.Polyalthia suberosa Thw. (from Assam to Uttar Pradesh in the North and Kerala in the South) is known as Chamkhirni. The leaves contain alpha-and beta-amyrin, lupeol, beta- sitosterol, stigmasterol and campes- terol. The stems and leaves contain the triterpene, suberosol, which showed anti-HIV replication activity. The stem bark contains alkaloids, oxostepha- nine and lanuginosine, which exhibited antibacterial activity against several Gram-positive and Gram-negative bacteria.... polyalthia longifoliaAction. Anti-stress, antiviral, adaptogen, aphrodisiac, vasodilator, hypoglycaemic, tonic, adrenal hormone stimulant, anti-toxic activity in chemotherapy. Beneficial for boosting the body’s natural defence system, to resist viruses, free-radical toxins and even radiation. Increases immune resistance.
Uses: Conditions related to stress. Improves capacity for mental and physical exertion, to revitalise a run- down constitution, shingles, myalgic encephalomyelitis (ME), atherosclerosis in heart and arterial conditions, increases cerebral circulation in the elderly, non-caffeine invigorator, depression from overwork, jet-lag, children – classroom stress, recovery from surgical operation, radiation injury, immune stimulant in cancer therapy. To increase fertility. Enables patient to tolerate higher doses of radiation. Counters nuclear reactor leakage. Inhibits HIV-1 replication in cells acutely or chronically infected. Preparations. Miscellaneous products available.
Tea. Quarter of a teaspoon powdered root to each cup boiling water. OR: dissolve 1-2 capsules in cup of boiling water, once daily.
Tablets/capsules. 150mg, one thrice daily.
General uses and contra-indications: see GINSENG (PANAX). ... ginseng - siberian
Action. Anti-infective against Coxsackie virus. Immune stimulant. Antiviral.
Uses: Myalgic encephalomyelitis (ME). Upper respiratory infection. For increased white blood cell count, improved sleep habits and to stimulate appetite in patients receiving chemotherapy and radiation. (American Health 1989 8th Oct. –100) To increase production of interferon. Gastric ulcer therapy. Influenza. The common cold. To combat Coxsackie B myocarditis. Of value for incontinence and frequency of urine. Inhibits HIV-1 replication in cells acutely or chronically infected.
Preparation. Decoction. Dried root: 2 teaspoons to each cup of water simmered gently 20 minutes. Half- 1 cup thrice daily. ... huang qi
Possible side effects of zidovudine include anaemia, which may be severe enough to require a blood transfusion, nausea, loss of appetite, and headache.
Zidovudine also impairs the absorption of trimethoprim and sulfamethoxazole, the antibiotic drugs used to treat pneumonia in people who have , thus reducing the effectiveness of these drugs.... yttrium
DNA (deoxyribonucleic acid) the genetic material of nearly all living organisms, which controls heredity and is located in the cell nucleus (see chromosome; gene). DNA is a *nucleic acid composed of two strands made up of units called *nucleotides (see illustration). The two strands are wound around each other into a double helix and linked together by hydrogen bonds between the bases of the nucleotides (see base pairing). The genetic information of the DNA is contained in the sequence of bases along the molecule (see genetic code); changes in the DNA cause *mutations. The DNA molecule can make exact copies of itself by the process of *replication, thereby passing on the genetic information to the daughter cells when the cell divides.... dmsa
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