Archive for the ‘Parasitology’ Category
Pattern of AIDS virus transmission
June 17th, 2011 | 
Author: The AIDS virus was found in human body fluids, and most commonly found in blood, semen and vaginal fluids. In other body fluids can also be found (such as fluid milk) but the amount is very small.
Amounting to 75-85% of transmission occurs through sexual contact (5-10% of them through homosexual relations), 5-10% due to contaminated syringes (primarily in injecting drug users), 3-5% through contaminated blood transfusions.
HIV infection, a majority (more than 80%) suffered by the productive age group (15-49 years), especially men, but women tend to increase the proportion of patients.
Infections in infants and children, 90% occurred from mothers with HIV. Approximately 25-35% of babies born by a mother with HIV will become infected with HIV, the infection occurred during pregnancy, during childbirth and through breastfeeding. With antiretroviral treatment in the last trimester of pregnancy, the risk of transmission can be reduced to only 8%.
TRAVEL INFECTION HIV / AIDS
When a person infected with the AIDS virus can take 5-10 years to get to the stage known as AIDS. After the virus into the human body, so long as 2-4 months of the existence of such viruses can not be detected by blood tests even though the virus itself is already present in the human body. This phase is called the window period. Before going on the stage of AIDS, HIV-positive person is named because there is HIV in their blood. At this stage of the HIV + physical state concerned does not have any complaints or specific disorders, and even can keep working as usual. In terms of transmission, so in this condition and preferably within the already active transmit the virus to others if she had sex or a blood donor.
Since the entry of the virus in the human body the virus could undermine the white blood cells (which play a role in the immune system) and after 5-10 years it will be destroyed and the body’s immune patients included in the AIDS stage where there is a variety of infections such as fungal infections, viral- Other viruses, cancer, etc.. Patients will die within 1-2 years later because of infection.
In industrialized countries, an adult who is infected with HIV will develop AIDS within 12 years, while in developing countries over a shorter time is 7 years old.
After becoming AIDS, the survival rate in industrialized countries could have been extended to 3 years, whereas in developing countries is still less than 1 year. This survival rate is closely linked to the use of antiretroviral drugs, treatment of opportunistic infections and better service quality.
The pattern of infection globally, approximately 90% of cases of HIV / AIDS in developing countries.
Current distribution is:
* Sub-Saharan Africa: 14 million
* South-East Asia: 4.8 million
* East Asia-Pacific: 35,000
* Middle East: 200,000
* Caribbean: 270,000
* Latin America: 1.3 million
* Eastern Europe – Central Asia: 30,000
* Australia: 13,000
* Western Europe: 470,000
* North America: 780,000
With globalization, the movement of population and economic growth, the epicenter of HIV / AIDS infection is currently shifting to Asia.
Malaria
We turn now to the world’s third largest infectious killer, which has taken its greatest toll among children, especially African children, living in poverty.
The Cost of Malaria
Malaria’s human toll is enormous. An estimated 250 million people suffer from malarial disease each year, and the disease annually kills between 1 million and 2.5 million people, mostly pregnant women and children under the age of 5. The poor disproportionately suffer the consequences of malaria: 58% of malaria deaths occur in the poorest 20% of the world’s population, and 90% are registered in sub-Saharan Africa. The differential magnitude of this mortality burden is greater than that associated with any other disease. Likewise, the morbidity differential is greater for malaria than for diseases caused by other pathogens, as documented in a study from Zambia that revealed a 40% greater prevalence of parasitemia among children under 5 in the poorest quintile than in the richest.
Despite suffering the greatest consequences of malaria, the poor are precisely those least able to access effective prevention and treatment tools. Economists describe the complex interactions between malaria and poverty from an opposite but complementary perspective: they delineate ways in which malaria arrests economic development both for individuals and for whole nations. Microeconomic analyses focusing on direct and indirect costs estimate that malaria may consume up to 10% of a household’s annual income. A Ghanaian study that categorized the population by income group highlighted the regressive nature of this cost: the burden of malaria represents only 1% of a wealthy family’s income but 34% of a poor household’s income.
At the national level, macroeconomic analyses estimate that malaria may reduce the per capita gross national product of a disease-endemic country by 50% relative to that of a nonmalarial country. The causes of this drag include high fertility rates, impaired cognitive development of children, decreased schooling, decreased saving, decreased foreign investment, and restriction of worker mobility. Given this enormous cost, it is little wonder that an important review by the economists Sachs and Malaney concludes that “where malaria prospers most, human societies have prospered least.”
SINEs
The two EhSINEs are clearly related to the EhLINEs, as they have a conserved 30 sequence. They are nonautonomous, non-LTR retrotransposons (nonautonomous SINEs). The genetic elements encoding the abundant polyadenylated but untranslatable transcripts found in E. histolytica cDNA libraries [initially designated interspersed elements (Cruz-Reyes and Ackers, 1992; Cruz-Reyes et al., 1995) or ehapt2 (Willhoeft et al., 2002)] have now been designated EhSINE1 (Van Dellen et al., 2002a; Willhoeft et al., 2002). BLAST searching of databases with representative examples of the first 44 EhSINE1s detected has identified 90 full-length (_99% complete) copies and at least a further 120 partial (_50% of full length) copies in the genome. Length variation is observed among EhSINE1s and is largely due to variable numbers of internal 26–27 bp repeats (J. P.Ackers, unpublished data). The majority contain 2 internal repeats and cluster closely around 546 bp in length. A second E. histolytica SINE (EhSINE2) has recently been described (Van Dellen et al., 2002a; Willhoeft et al., 2002). Examination of the 4 published sequences again suggests the presence of variable numbers of short (20 bp) imperfect repeats. BLAST searching identified a total of 47 fulllength (_99%) and at least 60 partial copies in the genome. The 30-end of EhSINE2 shows high similarity (76%) to the 30 end of EhLINE2. A polyadenylated transcript designated UEE1 found commonly in cDNA libraries from E. dispar (Sharma et al., 1999) is also a non-LTR retrotransposon. A single copy of a UEE1-like element has been identified in the E. histolytica genome and is here designated EhSINE3. There is no significant sequence identity between EhSINE3 and EhLINE3, but the 30 end of EhSINE3 is very similar to that of EhLINE1. Analysis of an E. histolytica EST library identified over 500 significant hits to both EhSINE1 and EhSINE2. No convincing transcript from EhSINE3 could be identified, although the nearly identical E. dispar UEE elements (EdSINE1; Shire and Ackers, 2007) are abundantly transcribed. A very abundant polyadenylated transcript, ehapt1, was described by Willhoeft et al. (1999) in a cDNA library. However, only a small number of partial matches could be found in the current E. histolytica assembly and only 10–20 strong hits in the much larger E. histolytica EST library now available. ehapt1 does not appear to be a SINE element, and its nature is currently unclear. The lack of matches in the genome suggests that either it is encoded in regions missing from the current assembly or it contains numerous introns.