Here is a link to the PDF Version where you can actually see the images. It is also colour coded to help with the more important words. http://dl.dropbox.com/u/42415439/HIV_Script.pdf
(HIV) - 3D
HIV stands for Human immunodeficiency virus; it is a member of the retrovirus family.
Retrovirology
Retroviruses replicates in their host using its own enzyme to produce DNA.
HIV causes acquired immunodeficiency syndrome which is a disease of the [Human immune system], this is a condition which progressive failure of the immune system allows life threatening infections and cancers to thrive.
HIV focuses on the human immune system and infects the vital cells such as helper T cells.
Now helper T cells are a sub-group of lymphocytes which are a type of white blood cell, that play an important role in the immune system. Particularly in the adaptive immune system, lymphocytes help the activity of other immune cells by releasing T cell cytokines
Diving further into our microscope lymphocytes can be divided into large and small lymphocytes, which look like
Single human lymphocyte Lymphocyte surrounded by red blood cells
These vital helper T Cells it infects are: macrophages and dendritic cells.
Macrophages are cells produced by the differentiation of monocytes in tissues and dendritic cells are immune cells forming part of the mammalian immune system.
Monophage stretching to engulf two particles/ possible pathogens .
What happens through HIV infection?
The infection leads to low levels of CD4 TCells through three main mechanisms:
First - Direct viral killing of infected cells
Second - Increased rates of apoptosis in infected cells; Apoptosis is he process of programmed cell death, which would then lead to the
Third mechanism - the killing of infected CD4 TCells by CD8 cytotoxic lymphocytes. A cytotoxic T cell is a type of white blood cell that kills cancer cells and cells that are infected especially with viruses, or cells that are damaged in other ways.
As the CD4 T cell numbers decline below a critical level; the cell-mediated immunity is lost, and the body becomes progressively more susceptible to opportunistic infections.
Structure and genome
HIV has a different structure from other retroviruses. Roughly spherical with a diameter of about 120 nanometers and around 60 times smaller than a red blood cell yet it is large for a virus.
HIV is composed of two copies of positive single-stranded ribonucleic acid or that codes for the virus's nine genes enclosed by a conical capsid composed of 2,000 copies of the viral protein.
HIV is composed of two copies of positive single-stranded ribonucleic acid or that codes for the virus's nine genes enclosed by a conical capsid composed of 2,000 copies of the viral protein.
Discovery
The first clinically observed cases of AIDS were in the United States in 1981. Initial cases were a drug users who used injections and gay men with no known cause of impaired immunity.
They showed symptoms of Pneumocystis carinii pneumonia PCP for short, which was a rare opportunistic infection known to occur in people with very compromised immune systems.
They showed symptoms of Pneumocystis carinii pneumonia PCP for short, which was a rare opportunistic infection known to occur in people with very compromised immune systems.
Soon after, additional gay men developed a previously rare skin cancer called Kaposi’s sarcoma KS for short. In the United States, many more cases of PCP and KS emerged, which alerted the Centers for Disease Control and Prevention and they formed a task force to monitor the outbreak.
Origins
Origins
HIV-1 and HIV-2 are believed to have both originated in non-human primates, in West-central Africa and were transferred to humans by a process known as zoonosis in the early 20th century.
HIV-1 appears to have originated in southern Cameroon through the evolution of, a Simian immunodeficiency virus SIV for short. It infects wild chimpanzees and HIV-1 descends from the SIV endemic in the chimpanzee subspecies.
HIV-2’s closest’s relative is a virus of the sooty mangabey, an old world monkey living in Litoral West Africa.
The new world monkeys such as the owl monkeys are resistant to HIV-1 infection, made possible by genomic fusion of two viral resistance genes.
HIV-1 is thought to have jumped the species barrier on at least three separate occasions, giving rise to the three groups of the viruses, the M, N, and O groups.
HIV-1 appears to have originated in southern Cameroon through the evolution of, a Simian immunodeficiency virus SIV for short. It infects wild chimpanzees and HIV-1 descends from the SIV endemic in the chimpanzee subspecies.
HIV-2’s closest’s relative is a virus of the sooty mangabey, an old world monkey living in Litoral West Africa.
The new world monkeys such as the owl monkeys are resistant to HIV-1 infection, made possible by genomic fusion of two viral resistance genes.
HIV-1 is thought to have jumped the species barrier on at least three separate occasions, giving rise to the three groups of the viruses, the M, N, and O groups.
Humans who participate in bushmeat activities, either as hunters or as bushmeat vendors gave rise to some evidence of acquiring SIV which was common. Bushmeat is referred to as the meat from wild animals witch are especially endangered or a protected species.
SIV is a weak virus, and it is typically suppressed by the human immune system within weeks of infection. The cognitive suggestion is that several transmissions of the virus from individual to individual in quick succession was the necessary step which allowed it enough time to mutate into HIV.
Due to its relatively low person-to-person transmission rate, it can only spread throughout the population in the presence of one or more of high-risk transmission channels, which are thought to have been absent in Africa prior to the 20th century.
These specific proposed high-risk transmission channels which allowed the virus to adapt to humans and spread throughout the society, depended on the proposed timing of the animal-to-human crossing. The Genetic studies of the virus suggest that the most recent common ancestor of the HIV-1 M group dates back to 1910.
Proponents of this dating link the HIV epidemic with the emergence of colonialism and growth of large colonial African cities, leading to social changes, including a higher degree of sexual promiscuity, the spread of prostitution, and the concomitant high frequency of genital ulcer diseases (such as syphilis) in nascent colonial cities.[89] While transmission rates of HIV during vaginal intercourse are low under regular circumstances they are increased many fold if one of the partners suffers from a sexually transmitted infection resulting in genital ulcers. Early 1900s colonial cities were notable due to their high prevalence of prostitution and genital ulcers to the degree that as of 1928 as many as 45% of female residents of eastern Kinshasa were thought to have been prostitutes and as of 1933 around 15% of all residents of the same city were infected by one of the forms of syphilis.[89]
SIV is a weak virus, and it is typically suppressed by the human immune system within weeks of infection. The cognitive suggestion is that several transmissions of the virus from individual to individual in quick succession was the necessary step which allowed it enough time to mutate into HIV.
Due to its relatively low person-to-person transmission rate, it can only spread throughout the population in the presence of one or more of high-risk transmission channels, which are thought to have been absent in Africa prior to the 20th century.
These specific proposed high-risk transmission channels which allowed the virus to adapt to humans and spread throughout the society, depended on the proposed timing of the animal-to-human crossing. The Genetic studies of the virus suggest that the most recent common ancestor of the HIV-1 M group dates back to 1910.
Proponents of this dating link the HIV epidemic with the emergence of colonialism and growth of large colonial African cities, leading to social changes, including a higher degree of sexual promiscuity, the spread of prostitution, and the concomitant high frequency of genital ulcer diseases (such as syphilis) in nascent colonial cities.[89] While transmission rates of HIV during vaginal intercourse are low under regular circumstances they are increased many fold if one of the partners suffers from a sexually transmitted infection resulting in genital ulcers. Early 1900s colonial cities were notable due to their high prevalence of prostitution and genital ulcers to the degree that as of 1928 as many as 45% of female residents of eastern Kinshasa were thought to have been prostitutes and as of 1933 around 15% of all residents of the same city were infected by one of the forms of syphilis.[89]
An alternative view holds that unsafe medical practices in Africa during years following World War II, such as unsterile reuse of single use syringes during mass vaccination, antibiotic and anti-malaria treatment campaigns, were the initial vector that allowed the virus to adapt to humans and spread.[87][90][91]
The earliest well documented case of HIV in a human dates back to 1959 in the Congo.[92] The virus may have been present in the United States as early as 1966.[93]
