AIDS

Acquired immune deficiency syndrome or acquired immunodeficiency syndrome (AIDS) is a disease of the human immune system caused by the human immunodeficiency virus (HIV).
This condition progressively reduces the effectiveness of the immune system and leaves individuals susceptible to opportunistic infections and tumors. HIV is transmitted through direct contact of a mucous membrane or the bloodstream with a bodily fluid containing HIV, such as blood, semen, vaginal fluid, preseminal fluid, and breast milk.[4][5]
This transmission can involve anal, vaginal or oral sex, blood transfusion, contaminated hypodermic needles, exchange between mother and baby during pregnancy, childbirth, breastfeeding or other exposure to one of the above bodily fluids.
AIDS is now a pandemic. In 2007, it was estimated that 33.2 million people lived with the disease worldwide, and that AIDS killed an estimated 2.1 million people, including 330,000 children. Over three-quarters of these deaths occurred in sub-Saharan Africa, retarding economic growth and destroying human capital.
Genetic research indicates that HIV originated in west-central Africa during the late nineteenth or early twentieth century. AIDS was first recognized by the U.S. Centers for Disease Control and Prevention in 1981 and its cause, HIV, identified in the early 1980s.
Although treatments for AIDS and HIV can slow the course of the disease, there is currently no vaccine or cure. Antiretroviral treatment reduces both the mortality and the morbidity of HIV infection, but these drugs are expensive and routine access to antiretroviral medication is not available in all countries. Due to the difficulty in treating HIV infection, preventing infection is a key aim in controlling the AIDS pandemic, with health organizations promoting safe sex and needle-exchange programmes in attempts to slow the spread of the virus. 

Cause

AIDS is the most severe acceleration of infection with HIV. HIV is a retrovirus that primarily infects vital organs of the human immune system such as CD4+ T cells (a subset of T cells), macrophages and dendritic cells. It directly and indirectly destroys CD4+ T cells.
Once HIV has killed so many CD4+ T cells that there are fewer than 200 of these cells per microliter (µL) of blood, cellular immunity is lost. Acute HIV infection progresses over time to clinical latent HIV infection and then to early symptomatic HIV infection and later to AIDS, which is identified either on the basis of the amount of CD4+ T cells remaining in the blood, and/or the presence of certain infections, as noted above.
In the absence of antiretroviral therapy, the median time of progression from HIV infection to AIDS is nine to ten years, and the median survival time after developing AIDS is only 9.2 months. However, the rate of clinical disease progression varies widely between individuals, from two weeks up to 20 years.
Many factors affect the rate of progression. These include factors that influence the body's ability to defend against HIV such as the infected person's general immune function. Older people have weaker immune systems, and therefore have a greater risk of rapid disease progression than younger people.
Poor access to health care and the existence of coexisting infections such as tuberculosis also may predispose people to faster disease progression. The infected person's genetic inheritance plays an important role and some people are resistant to certain strains of HIV. An example of this is people with the homozygous CCR5-Δ32 variation are resistant to infection with certain strains of HIV. HIV is genetically variable and exists as different strains, which cause different rates of clinical disease progression.
Sexual transmission
Sexual transmission occurs with the contact between sexual secretions of one person with the rectal, genital or oral mucous membranes of another. Unprotected receptive sexual acts are riskier than unprotected insertive sexual acts, and the risk for transmitting HIV through unprotected anal intercourse is greater than the risk from vaginal intercourse or oral sex.
However, oral sex is not entirely safe, as HIV can be transmitted through both insertive and receptive oral sex. Sexual assault greatly increases the risk of HIV transmission as condoms are rarely employed and physical trauma to the vagina or rectum occurs frequently, facilitating the transmission of HIV.
Other sexually transmitted infections (STI) increase the risk of HIV transmission and infection, because they cause the disruption of the normal epithelial barrier by genital ulceration and/or microulceration; and by accumulation of pools of HIV-susceptible or HIV-infected cells (lymphocytes and macrophages) in semen and vaginal secretions. Epidemiological studies from sub-Saharan Africa, Europe and North America suggest that genital ulcers, such as those caused by syphilis and/or chancroid, increase the risk of becoming infected with HIV by about fourfold. There is also a significant although lesser increase in risk from STIs such as gonorrhea, chlamydia and trichomoniasis, which all cause local accumulations of lymphocytes and macrophages.
Transmission of HIV depends on the infectiousness of the index case and the susceptibility of the uninfected partner. Infectivity seems to vary during the course of illness and is not constant between individuals. An undetectable plasma viral load does not necessarily indicate a low viral load in the seminal liquid or genital secretions.
However, each 10-fold increase in the level of HIV in the blood is associated with an 81% increased rate of HIV transmission. Women are more susceptible to HIV-1 infection due to hormonal changes, vaginal microbial ecology and physiology, and a higher prevalence of sexually transmitted diseases.
People who have been infected with one strain of HIV can still be infected later on in their lives by other, more virulent strains.
Infection is unlikely in a single encounter. High rates of infection have been linked to a pattern of overlapping long-term sexual relationships. This allows the virus to quickly spread to multiple partners who in turn infect their partners. A pattern of serial monogamy or occasional casual encounters is associated with lower rates of infection.
HIV spreads readily through heterosexual sex in Africa, but less so elsewhere. One possibility being researched is that schistosomiasis, which affects up to 50 per cent of women in parts of Africa, damages the lining of the vagina.
Exposure to blood-borne pathogens
This transmission route is particularly relevant to intravenous drug users, hemophiliacs and recipients of blood transfusions and blood products. Sharing and reusing syringes contaminated with HIV-infected blood represents a major risk for infection with HIV.
Needle sharing is the cause of one third of all new HIV-infections in North America, China, and Eastern Europe. The risk of being infected with HIV from a single prick with a needle that has been used on an HIV-infected person is thought to be about 1 in 150 (see table above). Post-exposure prophylaxis with anti-HIV drugs can further reduce this risk.
This route can also affect people who give and receive tattoos and piercings. Universal precautions are frequently not followed in both sub-Saharan Africa and much of Asia because of both a shortage of supplies and inadequate training.
The WHO estimates that approximately 2.5% of all HIV infections in sub-Saharan Africa are transmitted through unsafe healthcare injections. Because of this, the United Nations General Assembly has urged the nations of the world to implement precautions to prevent HIV transmission by health workers.
The risk of transmitting HIV to blood transfusion recipients is extremely low in developed countries where improved donor selection and HIV screening is performed. However, according to the WHO, the overwhelming majority of the world's population does not have access to safe blood and between 5% and 10% of the world's HIV infections come from transfusion of infected blood and blood products.
Perinatal transmission
The transmission of the virus from the mother to the child can occur in utero during the last weeks of pregnancy and at childbirth. In the absence of treatment, the transmission rate between a mother and her child during pregnancy, labor and delivery is 25%.
However, when the mother takes antiretroviral therapy and gives birth by caesarean section, the rate of transmission is just 1%. The risk of infection is influenced by the viral load of the mother at birth, with the higher the viral load, the higher the risk. Breastfeeding also increases the risk of transmission by about 4 %. 

Misconceptions

A number of misconceptions have arisen surrounding HIV/AIDS. Three of the most common are that AIDS can spread through casual contact, that sexual intercourse with a virgin will cure AIDS, and that HIV can infect only homosexual men and drug users. Other misconceptions are that any act of anal intercourse between gay men can lead to AIDS infection, and that open discussion of homosexuality and HIV in schools will lead to increased rates of homosexuality and AIDS. 

Pathophysiology

 The pathophysiology of AIDS is complex, as is the case with all syndromes. Ultimately, HIV causes AIDS by depleting CD4+ T helper lymphocytes. This weakens the immune system and allows opportunistic infections. T lymphocytes are essential to the immune response and without them, the body cannot fight infections or kill cancerous cells. The mechanism of CD4+ T cell depletion differs in the acute and chronic phases.

During the acute phase, HIV-induced cell lysis and killing of infected cells by cytotoxic T cells accounts for CD4+ T cell depletion, although apoptosis may also be a factor. During the chronic phase, the consequences of generalized immune activation coupled with the gradual loss of the ability of the immune system to generate new T cells appear to account for the slow decline in CD4+ T cell numbers.
Although the symptoms of immune deficiency characteristic of AIDS do not appear for years after a person is infected, the bulk of CD4+ T cell loss occurs during the first weeks of infection, especially in the intestinal mucosa, which harbors the majority of the lymphocytes found in the body. The reason for the preferential loss of mucosal CD4+ T cells is that a majority of mucosal CD4+ T cells express the CCR5 coreceptor, whereas a small fraction of CD4+ T cells in the bloodstream do so.
HIV seeks out and destroys CCR5 expressing CD4+ cells during acute infection. A vigorous immune response eventually controls the infection and initiates the clinically latent phase. However, CD4+ T cells in mucosal tissues remain depleted throughout the infection, although enough remain to initially ward off life-threatening infections.
Continuous HIV replication results in a state of generalized immune activation persisting throughout the chronic phase. Immune activation, which is reflected by the increased activation state of immune cells and release of proinflammatory cytokines, results from the activity of several HIV gene products and the immune response to ongoing HIV replication. Another cause is the breakdown of the immune surveillance system of the mucosal barrier caused by the depletion of mucosal CD4+ T cells during the acute phase of disease.
This results in the systemic exposure of the immune system to microbial components of the gut’s normal flora, which in a healthy person is kept in check by the mucosal immune system. The activation and proliferation of T cells that results from immune activation provides fresh targets for HIV infection. However, direct killing by HIV alone cannot account for the observed depletion of CD4+ T cells since only 0.01–0.10% of CD4+ T cells in the blood are infected.
A major cause of CD4+ T cell loss appears to result from their heightened susceptibility to apoptosis when the immune system remains activated. Although new T cells are continuously produced by the thymus to replace the ones lost, the regenerative capacity of the thymus is slowly destroyed by direct infection of its thymocytes by HIV. Eventually, the minimal number of CD4+ T cells necessary to maintain a sufficient immune response is lost, leading to AIDS
Cells affected
The virus, entering through which ever route, acts primarily on the following cells:
•    Lymphoreticular system:
o    CD4+ T-Helper cells
o    Macrophages
o    Monocytes
o    B-lymphocytes
•    Certain endothelial cells
•    Central nervous system:
o    Microglia of the nervous system
o    Astrocytes
o    Oligodendrocytes
o    Neurones – indirectly by the action of cytokines and the gp-120
The effect
The virus has cytopathic effects but how it does it is still not quite clear. It can remain inactive in these cells for long periods, though. This effect is hypothesized to be due to the CD4-gp120 interaction.
•    The most prominent effect of HIV is its T-helper cell suppression and lysis. The cell is simply killed off or deranged to the point of being function-less (they do not respond to foreign antigens). The infected B-cells can not produce enough antibodies either. Thus the immune system collapses leading to the familiar AIDS complications, like infections and neoplasms (vide supra).
•    Infection of the cells of the CNS cause acute aseptic meningitis, subacute encephalitis, vacuolar myelopathy and peripheral neuropathy. Later it leads to even AIDS dementia complex.
•    The CD4-gp120 interaction (see above) is also permissive to other viruses like Cytomegalovirus, Hepatitis virus, Herpes simplex virus, etc. These viruses lead to further cell damage i.e. cytopathy.
Molecular basis
For details, see:
•    Structure and genome of HIV
•    HIV replication cycle
•    HIV tropism

Raja Ravi Varma

Raja Ravi Varma, (April 29, 1848- October 2, 1906) was an Indian painter from the princely state of Travancore who achieved recognition for his depiction of scenes from the epics of the Mahabharata and Ramayana. His paintings are considered to be among the best examples of the fusion of Indian traditions with the techniques of European academic art.
Varma is most remembered for his paintings of beautiful sari-clad women, who were portrayed as shapely and graceful. His exposure in the west came when he won the first prize in the Vienna Art Exhibition in 1873. Raja Ravi Varma died in 1906 at the age of 58. He is considered among the greatest painters in the history of Indian art.

“Moving from Trivandrum to Kilimanoor was quite a dramatic moment in my life. But for me the highlight everyday was a visit to the Kilimanoor Kottaram (palace) where Bhavani Tamburati (Princess Bhavani) would teach me to play Veena show me the studio that was used by Raja Ravi Verma. Often I would meet Mangala Bai Tamburati the sister of Raja Ravi Verma who at the age of 80 was a brilliant Veena artist and great painter”. I must have heard my mother say this a hundred times as she talked about the time her father decided to quit the urban life and move to this quiet village in the 1940s.

There must be something about this village for it produced one of the greatest painters of India. Raja Ravi Varma was born on April 29, 1848 at Kilimanoor. As a boy of five, he filled the walls of his house with pictures of animals and illustrations from everyday life. His uncle the artist Raja Raja Varma recognized his talents and gave him elementary art lessons. He was taken to Thiruvananthapuram in his fourteenth year to stay in the royal palace and learn oil painting.  During these formative years the young Ravi Varma had many opportunities to discover and learn new techniques and media in the field of painting. His later years spent in Mysore, Baroda ad other parts of the country enabled him to sharpen and expand his skills and blossom into a mature and complete painter.

While he was certainly a “Raja” or a Prince by birth, I learned from my  mother’s description of the life of the Kerala princes especially in Killimanore was fairly simple. It was not at all ostentatious by any stretch of the imagination. Their meals were simple made of roots and fruits available locally. But their generosity of heart  was amazing as was their dedication to the arts. The major activity of the day was being tutored by a brilliant teacher "Madhavar" on music, practising Veena and painting. Ofcourse this was done not with any intention of stage performances but rather for the upliftment of the soul.

Raja Ravi Varma owed his success to a systematic training, first in the traditional art of Thanjavoor, and then in European art. His paintings can be broadly classified into 1.Portraits, 2.Portrait-based compositions, 3.Theatrical compositions based on myths and legends. Ravi Varma is considered as modern among traditionalists and a rationalist among moderns. He provided a vital link between the traditional Indian art and the contemporary between the Thanjavoor School and Western Academic realism.  He brought Indian painting to the attention of the larger world.

Ravi Verma is an artist who is credited with bringing about a momentous turn in the art of India, influencing future generations of artists from different streams. He was the first artist to cast the Indian Gods and mythological characters in natural earthy surroundings using a European realism; a depiction adopted not only by the Indian “calendar-art”- spawning ubiquitous images of Gods and Goddesses, but also by literature and later by the Indian film industry- affecting their dress and form even today.

Learning to paint was not easy. The medium was very new and the technique equally elusive in those days. Only one person in Travancore knew the technique of oil painting - Ramaswamy Naicker of Madura, who, recognizing a potential rival in Varma, refused to teach him the know-how. Naicker's student, Arumugham Pillai would actually sneak into Moodath Madam at nightfall to share his knowledge with Varma, against his teacher’s wishes.      Bhishma abdicating his right to the throne to get the fisher girl's hand for his father Shantanu

This clandestine education was only supplemented by watching a visiting Dutch portrait artist who painted the portraits of Ayilyam Thirunal and his wife. Through trial, error and hard work, Ravi Varma worked with the pliable medium, learning to blend, smooth and maneuver the flexibility that was afforded by this slow drying substance.

When Varma himself painted the portraits of this royal couple, this self-taught artist’s blazing talent far outshone the Dutchman! Ravi Varma’s creativity was further tampered by listening to the music of veterans, watching Kathakali, going through the manuscripts preserved in ancient families and listening to the artistic interpretations of the epics. He firmly believed in the hollistic approach to art, in the true Indian style.

Ravi Varma’s fame as a portrait artist soared with several important portrait commissions from the Indian aristocracy and British officials between 1870 and 1878, and the sensitivity and immense competence this artist still remains unsurpassed. His clever portrayal would add elegance to the personality of the protagonist, like unmasking the fragrance of a flower. The small town of Kilimanoor was compelled to open a post office, as letters with requests for paintings arrived from every where. The recognition that Ravi Varma received in major exhibitions abroad was for the portrait-based renditions, which were meticulous compositions of people, their demeanor and attires.
In 1873 he won the first prize at the Madras Painting Exhibition and he became a world famous Indian painter after winning in 1873 Vienna Exhibition. Though not really qualified for the title of a Raja, when an imperial citation happened to come across in the name of Raja Ravi Varma, the name stuck and stayed.

With oil paints applied thickly, Ravi Varma created lustrous, impasted jewellery, brocaded textures, and subtle shades of complexions. Though several folk and traditional art forms of India since time immemorial subsisted as illustrations for religious narratives, yet, illusionist paintings as a medium for story telling was Ravi Varma’s invention. He cleverly picked the particularly touching stories and moments from the Sanskrit classics.

Ravi Varma was convinced that mass reproduction of his paintings would initiate millions of Indians to real Art, and in 1894 he set up an oleography press called the Ravi Varma Pictures Depot. For photo-litho transfers, the Pictures Depot relied on Phalke's Engraving & Printing whose proprietor, Dhundiraj Govind Phalke, became famous as Dadasaheb of Indian Cinema a few years later.

While Raja Ravi Verma has long since left the world, his creations depicting stories and characters from another world has forever remained etched in our hearts.

Raja Rvivarma's paintings

The Creation of Adam

The Creation of Adam is a section of Michelangelo's fresco Sistine Chapel ceiling painted circa 1511. It illustrates the Biblical story from the Book of Genesis in which God the Father breathes life into Adam, the first man. Chronologically the fourth in the series of panels depicting episodes from Genesis on the Sistine ceiling, it was among the last to be completed. 

Composition 

God is depicted as an elderly bearded man wrapped in a swirling cloak while Adam, on the lower left, is completely naked. God's right arm is outstretched to impart the spark of life from his own finger into that of Adam, whose left arm is extended in a pose mirroring God's, a reminder that man is created in the image and likeness of God (Gen 1:26). Another point is that Adam's finger and God's finger are not touching. It gives the appearance that God, the giver of life, is reaching out to Adam and Adam is receiving. The pink backdrop behind God is in the shape of a brain. Michelangelo may have used this symbol to show God's plan of creation which had not yet been revealed to the first man.
The inspiration for Michelangelo's treatment of the subject may come from a medieval hymn called Veni Creator Spiritus, which asks the 'finger of the paternal right hand' (digitus paternae dexterae) to give the faithful speech, love and strength. 

Anatomical theories  

Several hypotheses have been put forward about the meaning of The Creation of Adam's highly original composition, many of them taking Michelangelo's well-documented expertise in human anatomy as their starting point. In 1990 a physician named Frank Lynn Meshberger noted in the medical publication the Journal of the American Medical Association that the background figures and shapes portrayed behind the figure of God appeared to be an anatomically accurate picture of the human brain, including the frontal lobe, optic chiasm, brain stem, pituitary gland, and the major sulci of the cerebrum. Alternatively, it has been observed that the red cloth around God has the shape of a human uterus (one art historian has called it a "uterine mantle"), and that the scarf hanging out, coloured green, could be a newly cut umbilical cord.