Older people less likely to be offered an HIV test in English sexual health clinics

Despite their mandate to offer HIV testing to all attendees, sexual health clinics in England are less likely to offer a test to older patients, according to an analysis of Public Health England data recently published in the International Journal of STD & AIDS.

Attendees in their late twenties had the highest likelihood of being offered HIV testing, with the proportion of attendees who were offered testing declining with increasing age.

In the 15-49 years age group, HIV testing was offered to 92% of men who have sex with men (MSM), 92% of heterosexual men and 85% of heterosexual women. For people aged over 50 years, offer rates fell to 88%, 85% and 78% respectively.

The decline in the offer of HIV testing was steepest for older heterosexual women. In those aged over 70 years, HIV testing was offered to 87% of MSM, 76% of heterosexual men and 52% of women.

While clinicians might be reluctant to offer a test because they think older patients are more likely to refuse, this concern is not backed up by the data. The strongest determinant of acceptance of the offer was sexual orientation.

  • Men who have sex with men: 96% of those under the age of 50 and 94% over 50 accepted the offer.
  • Heterosexual men: 85% of those under 50 and 83% of those over 50 accepted the offer.
  • Heterosexual women: 75% of those under 50 and 77% of those over 50 accepted the offer.

Low rates of HIV testing among older patients in primary care and other general health settings might be explained by clinicians not seeing sexual health as relevant in this age group, or expecting their older patients to be uncomfortable talking about sexually transmitted infections. However, this should not be a factor when older people attend sexual health clinics.

National and international HIV testing guidelines recommend that all people attending sexual health clinics are offered an HIV test. Moreover, people over the age of 50 are more likely to be diagnosed with HIV at a late stage, with a CD4 cell count below 350 cells/mm3, than younger people.

The figures come from 1.4 million attendance records from sexual health clinics in 2014. A comparison of the years between 2009 and 2014 did show some improvement over time, but the lower rate of HIV testing in older people is likely to contribute to late diagnosis in this age group.

Pastor demands couple undergo three HIV tests on wedding day, and still cancelled it

Pastor demands couple undergo three HIV tests on wedding day, and still cancelled it

A local pastor who declined to officiate a wedding ceremony in Bahati area, Nakuru County on Saturday has defended himself saying the couple did not meet the standards set by his church.

Joyce Waithera and her fiance Paul Waithaka are said to have arrived at the Mizpah House of Prayer church in good time, ready to walk down the isle and recite their wedding vows. Friends and family members had gathered early in what was expected to be a glamorous wedding.

But upon arrival, the couple was summoned by the head of the church, Apostle Jesse Karanja, to his office where he reportedly instructed them to undergo a HIV test and return to him with their results.

Never mind that this was at 1 o’clock in the afternoon hours after the two expected to have been married.

They returned and the results were negative. Waithera had also been asked to do a pregnancy test and the results were also negative.

According to family members, the officiating minister kept the couple waiting again until 4pm, where he instructed them to undergo yet another test. They did, and the results were negative.

Frustrated, the Apostle asked them to do a third test, this time at a clinic of his choice. The couple obeyed, but this time the results allegedly indicated that the bride was HIV positive and that she was pregnant.

The results shocked them but they were still hopeful that they would continue with the ceremony, after all their status would remain their secret, but the Apostle appears to have had other things up his sleeves.

He again kept the couple and the guests waiting until 6pm and only emerged from his office saying he cannot officiate the wedding because the law does not allow weddings to be conducted past 6pm.

The couple drove away in a huff leaving behind family members and guests to feast on the meals that had been prepared.

Speaking while delivering his sermon on Sunday, Apostle Karanja defended his action saying the couple failed to meet the set standards.

“Basic principles of our Christian Pentecostal ministry were not met. As an apostolic leader I have to answer to God about your life… I have the authority to tell you, ‘you must go this way.” If you don’t do it I have a legal authority from heaven to ex-communicate you,” said Apostle Karanja.

“Yesterday, we were supposed to have a wedding but it did not happen. The main reason is that our standards as a Christian church organization were not met. Every member must adhere to some basic christian standards. Any deviation calls for the church not to perform any christian ordinance.

“We had given the couple up to Friday to fulfill some standard requirements of this ministry because we proclaim living a life of purity. We advocate sex out of marriage for young people. We have set our own biblical standards that everyone must meet. There are other personal reasons that we cannot give you,” said the clergy man.

The bridegroom’s father faulted the pastor for his actions, adding that his son had been a member of the church for the last six years.

“Even if he hates this young man, he should not have done that. This man has been a member of the his church for the last six years. He has really heartbroken this young couple. His actions are very suspicious, ” said the groom’s father.

The Apostle’s actions have now raised eyebrows about some church leaders’ role when it comes to their flocks’ medical conditions.

Despite spending close to one millions shillings for ceremony that did not go as planned, the couple says it will still go on with their plans and marry at a later date.

HIV tests can now be done at home

People will now be able to test for the disease at home

Digital sexual and reproductive health social enterprise, SH:24 has announced that it will be offering free HIV self-tests that can be done at home.

SH:24 has produced over 200,000 STI self-test kits since 2015 and has won awards for its service.

Now, SH:24 is providing free HIV testing to better understand what influences an individual when choosing a testing kit.

There are currently two types of self-test kits for HIV, one involves taking a prick of blood from a finger and will provide results in 15 minutes. The other involves the individual providing 15 drops of blood in a tiny pot and returning it to the lab.

Those who take the test will be asked to fill out a short survey, the data from which will be used to inform future HIV prevention research and service development at SH:24.

Individuals who choose to take the self-test at home will receive their results via text or over the phone by one of SH:24’s trained clinicians. Where necessary, patients will be referred for further treatment.

Everyone who takes the home test will receive a follow up call from an SH:24 employee offering advice.

Alongside the test, SH:24 offers 24 hour support for individuals.

HIV treatment has improved dramatically during recent years with huge strides being made in testing and treatment. According to Public Health England in 2016 new HIV diagnoses decreased, despite the same levels of testing. Home testing has helped with this progress.

HIV Prevention: Bridging The Gap Between Research And Impact

We are at an incredible moment in the history of the HIV/AIDS response, which reflected in the vibrancy of the HIV Research for Prevention (HIVR4P 2018) – the only global scientific conference focused on the fast-growing field of biomedical HIV prevention research. Today, the latest research in different areas of biomedical HIV prevention, including vaccines, rings, microbicides and other female-controlled forms of prevention, pre-exposure prophylaxis (PrEP) and long-acting delivery systems, offer the greatest promise of significantly slowing the toll of the disease.

And yet we are far away from ending the AIDS epidemic by 2030, and are also falling short of achieving the 90-90-90 UNAIDS targets by 2020.

While there has been immense progress in the field of HIV science, we are yet to see its public health impact on the ground.

“It is not just about R&D but about R&D and D – research and development, and delivery. If you take any one of those three letters out, we fail. Each of them is equally important. Undoubtedly, it is difficult to successfully complete the clinical study for a new product, but delivering that product to the people for whom it was designed, is harder.

Whether it is the ARVs, PrEP, vaginal rings, multipurpose prevention tools like the female condom, we see a huge gap in delivery”, said Mitchell Warren, Executive Director of AVAC, in an exclusive interview given to CNS onsite at the HIVR4P Conference being held in Madrid.


Till to date, more than 35 million people have died of HIV-related illnesses, and another 37 million people are living with HIV worldwide. In 2017 alone there were 1.8 million new infections (87,580 in India) and 940,000 deaths (69,110 in India). Governments have promised to end AIDS by 2030.

But the new cases graph is not dipping towards that steeply enough. Why are we failing to prevent new HIV transmissions?

According to Mitchell, “We are failing for a number of reasons. One is our failure to translate science into programmes fast enough. The second is the fundamental failure of the system in which people who need prevention and treatment most are least likely to be able to access it. To bridge this wide access gap we need to do two things simultaneously. We clearly need additional prevention options.

But more importantly, we need to simultaneously focus on our (delivery) systems. Countries need to build prevention programmes that respect people’s choices and needs and are capable to deliver any new prevention method. If there is anything we need to do differently, it is that we need to listen to the people who are in need of the product(s).

We have to act upon what people want, when they want and how they want it. We have to listen to them in their diversity and respect their different choices. One size will never fit all. A successful HIV/AIDS response is the one that takes in all the imperfect things we have and bundles them together in the most perfect programme.”


Women seem to be shortchanged as far as their own sexual and reproductive health is concerned. This is true not just in HIV prevention but for many other public health issues as well. Mitchell laments that even though sexuality is a part of human nature, people are scared to talk about sex. They are not comfortable about letting women make choices about what they want to put in their vagina.

“We want young women to have choices. But more often than not (we know this from reproductive health programmes) those choices are made by governments, by health providers and by their male partners— whether they can use an injectable contraceptive or the pill or an implant. Despite having so many wonderful family planning options, women cannot choose the one they want.

Many times their public health programme offers them just one or two choices because those who dictate their choices are often men. So, patriarchy, coupled with moralizing conservative governments, creates a complex ecosystem. But we need to inform people better, rather than moralise.

We need to talk about the female initiated prevention options and let the product user decide for herself. In fact, all adults, irrespective of their age or sex, should be free to make informed choices about which product to use for the benefit of their own health and not be influenced by their partners, peers, parents or by the moralising politicians, health providers and clinicians”, he says.


People know that HIV is no longer a death sentence, that they can get a pill everyday and live healthy and long, and not infect others once they have undetectable viral load. This is an empowering and important message. But if not communicated properly, it could have unintended consequences of making individuals and governments complacent that getting HIV is no big deal. Let us not forget that HIV still is a big deal. It is an epidemic.

Even though we can treat it, but the more people are infected, the harder it would be to treat them all from a financial perspective. We have to stop new infections. So we got to find the right balance to not scare people, not stigmatise PLHIV, but at the same time make them realise that being HIV free is possible and is important.

Mitchell’s sane advice is to be laser sharp in our focus – not only around new technologies, but also upon the programmes and infrastructure that can deliver a whole range of products. We need to do both— technology development and building systems that address the fundamental structural barriers—in a comprehensive, integrated and sustained way.

If we do one and not the other, we cannot end the AIDS epidemic. We have to create a demand for all the available effective prevention tools and make all of them available to people so that they can choose what suits their needs best. But all this has to be in an ecosystem where one can talk about sex and about prevention of HIV in a human rights based comfortable way.

Documentary ‘Lovesick’ revolves around love story of HIV couples

Documentary 'Lovesick' revolves around love story of HIV couples

Two US-based filmmakers, Ann S. Kim and Priya Giri Desai, have made a documentary titled “Lovesick” which revolves around the love story of an HIV positive couple. As the documentary had its India premiere at the 20th Jio MAMI Mumbai Film Festival, the makers said they wanted to explore the universal condition of all HIV patients through an Indian story.

The story of “Lovesick” revolves around the journey of Suniti Solomon, a doctor who started working with HIV-affected sex workers and slowly realised how people from different walks of life who are suffering from the disease live a miserable life of a loner as they cannot get married due to their condition.

Therefore, the Chennai-based doctor decided to start a matchmaking service for AIDS patients so that at least they can live happily with a life partner.

On what intrigued them to make the film, Kim told IANS here: “Two very important elements for a documentary film is character and access to the story. Dr Suniti Solomon has a wonderful personality and she was very open to life. So when we got to know the story, we wanted to explore the world of HIV Positive patients differently.”

“Yes, we intended to discover that world but we looked for something very universal that will not only be limited to Indian audience but globally, with its relatability,” added Desai.

The filmmakers shot Solomon’s journey for eight years and found her story from her son, who is Desai’s friend.

Set in southern India, the documentary’s narration juxtaposes the traditional rules of arranged marriage that focuses on social status and astrology, different from what Solomon believed is important — medical history to be sure that none of the potential bride and groom is HIV positive.

Was that a conscious decision?

Kim said: “When we were waiting to interact with some HIV positive patients, we were just observing people and having a quick chat with them. We were trying to explore their idea and thought on marriage — why is it so important for an Indian society to get married and what are the rules that they follow, because back in the US, we go little easy on these rules.”

“When we asked a few question on marriage to a majority of orthodox people, those are the natural reactions we have got,” she added.

The story ends as a love story between two AIDS patients — Manu and Kathik, courtesy Solomon who was instrumental in their match-making.

Whether they believe in them or not, the fact is Manu and Karthik felt the pressure of following those rules.

“Though it was not our agenda to take the reference of those 12 rules and position them opposite the viewpoint of Dr Solomon, we attempted to utilise these elements to structure our narration.”

“You know handling HIV positive is no big deal, handling the social stigma that is attached with it is difficult for patients”, said Desai, who was born in a South Indian Brahmin family but brought up in California.

The film has been nominated under the ‘Discovering India’ category at the MAMI Mumbai Film Festival, and it is the only documentary film in the nominees, which include feature films like “Rajma Chawal”, “Chippa” and “Namdev Bhau”.

Filming the heart-warming documentary was a sweet-bitter experience for the director duo, Desai made an interesting point about their on-field experience.

“In Chennai, when I was interacting with the locals, they would not open up easily, maybe because I am an Indian coming from the US. But whenever Kim was talking, since she is a foreigner, people would voluntarily talk about our culture without any hesitation. I would say her presence in our crew worked in our favour to set the story close to reality,” shared Desai.

Kim is a Korean brought up in the US. Asked if she discovered anything new about India during the filming of “Lovesick”, Kim said: “After my college, I actually came to India and travelled mostly in the northern side. This time when we were filming, I explored the southern part.

“Maybe I liked south Indian food a little more than north Indian food, which is spicy,” she quipped.

While Kim did not find India very exotic and unfamiliar, she said: “There is a certain similarity we find in the Asian society. Our family and social cultures are somewhere similar and that is why I did not feel out of place.”

Why Does Only One Type of HIV Cause Almost All Infections in India?

Why Does Only One Type of HIV Cause Almost All Infections in India?

The reason HIV-1C is the most common cause of the estimated 2.1 million HIV infections reported in India and half of all global infections is being unraveled. Scientists found that it stays on its relentless march by making two copies of an important region of a protein, according to a study published in the Journal of Biological Chemistry.

“Our work examines one unique molecular trick HIV-1C appears to use towards replication fitness,” says Udaykumar Ranga, lead author and a professor at HIV-AIDS Laboratory, Molecular Biology and Genetics Unit, Jawaharlal Nehru Centre for Advanced Scientific Research, Bengaluru.

“HIV-1C can efficiently duplicate certain regions of its genome to gain replication advantages unlike all other genetic families of HIV-1.”

Its M.O., mojo and moxie

HIV – the human immunodeficiency virus – is so versatile that researchers working with it cannot but marvel at its stealth. As Ranga explains effusively, it demonstrates many unique properties that no other pathogenic organism – viruses, yeast, fungi, protozoa or bacteria – can.

Off the blocks, HIV is highly proliferative. Every single unit churns out 10-100 billion new daughter viral particles every day. Even if 99% of these new viral particles are defective, what is left is still an enormous infectious population of HIV (1% = 100 million to 1 billion).

What’s more, Ranga says, “the virus does not pay for this extraordinary rate of proliferation.”

Secondly, it can also spawn unprecedented levels of genetic variation. HIV intentionally introduces errors into its daughter virions (viral particles) to make them all different from one another, which may make a large proportion of the new viruses defective. But this helps fight off threats from the immune system of a new recipient or a new drug discovered only a week ago, or even a drug yet to be discovered.

“The viral population is huge and diverse to counter any adverse condition, with a subpopulation readily having a survival advantage,” Ranga explains.

To top it off, it sits and hides, and lurks in the chromosomes in the nucleus – called chromatin – unseen by and inaccessible to the immune system, vaccines and drugs. No other pathogen is known to use this molecular strategy.

“The immune system is not designed to find a virus hiding in the chromatin,” according to Ranga. “There are many additional strategies HIV employs towards replication fitness.”

The HIV-1 families

HIV-1 is not one. It’s a hive. Its genetic variation is humungous. It works with intention, seemingly endowed with a mind of its own.

As Ranga puts it, sort of “like the Indian caste system – a caste to sub-caste to sub-sub-castes and on and on.” HIV-1 has many genetic families, approximately nine primary families (A through K) and a large number of recombinant forms. Each of these families can be divided into sub-families and sub-sub-families.

Of these genetic families, the one denoted ‘subtype C’ is the most important one because it causes half of all the infections in the world. Nearly all of the HIV infections of India are due to HIV-1C, and genetic families such as  A, B, D, E and others are not in India. In the West, family B dominates.

The viral family of subtype C dominates India, China, and Africa. It is also so variegated that the Indian HIV-1C strains may differ from the South African HIV-1C strains at the phylogenetic level. It shows its extraordinary capacity to adapt to the available environmental conditions, and Ranga reckons there must be a molecular basis underlying this success, known as replication fitness.

“It will be technically difficult, even impossible, to ascertain a single reason underlying the epidemiological success because many independent factors may contribute towards a specific characteristic simultaneously, each factor making a partial contribution to the gross total. The intrinsic molecular qualities, a founder effect (‘the first arrived’ has an advantage), the host factor landscape and the like all could make a difference,” Ranga says.

His lab examines the first factor: the intrinsic molecular properties of HIV-1C. Despite all the geographical variations, “all the HIV-1C viral strains appear to bring about an important change in the Gag protein to gain a major proliferative advantage.”

Clueing in on the PTAP motif

When Ranga and his team began nearly 15 years ago, he says he was surprised to see new viral variants emerging only or mostly in the HIV-1C family. Among other things, the lab focused on the causes underlying the dominance of subtype C, specifically if subtype C viruses isolated from HIV patients in India have molecular features that differ from other subtypes found in India or other countries.

As Prabhu Arunachalam, one of the study’s co-authors and now a postdoc in the US, narrates, they screened 56 HIV-infected people from India who were not being medicated.

When they sequenced the viruses thus obtained, the majority of the patients seemed to be harbouring ones with genomes of an expected length. However, eight people had viruses that had a small region called the ‘PTAP motif’ duplicated.

A motif, Arunachalam explains, is a small stretch of DNA sequence that is characteristic of a certain biological function.

For instance, PTAP – i.e. the amino acid sequence proline-threonine-alanine-proline, in that order – motif helps in the budding of viruses from cells. This motif is present in HIV-1 as well as several other retroviruses. But the function of this motif in all the viruses is the same: to help viral budding.

“The PTAP motif achieves this by recruiting proteins that transport the virus out of a cell,” Arunachalam says. In this way, the virus uses cell-sorting machinery to jump out of the cell and infect new cells.

To determine the range of viral budding, they first analysed the samples with a lower power technique (Sanger sequencing) and next with next-generation sequencing. The latter costs more money and so it was not done on all 56 samples in the beginning.

The analysis showed that the new variant viral strains containing duplication – i.e. double-PTAP viral strains – dominated the original single PTAP viral strains. About 70-99% of the viral strains in the blood were double PTAP-strains in almost all the subjects, at multiple follow-up times up to 30 months.

“This proved that HIV containing two PTAP domains has a great replicative advantage over the strains containing only one domain,” says Ranga.

According to Arunachalam, the finding suggests two important things. One: Viruses are evolving in patients who are not on medicines. Two: Once a virus duplicates this motif, it becomes the fittest and takes over within a period of six months (in the study, this was the time period after which each sample was taken).

Ranga thinks the dominant viral strain – the double-PTAP viral strain – is more likely to be transmitted to new people. He adds a caveat that they cannot say for sure because “survival advantage in individual subjects need not necessarily translate to spreading advantage in a population because additional selection forces operate in the population which are absent in individuals.”

“Nevertheless, the chances of replication advantage are expected to be higher at the population level if this is the case at the subject level.”

They also constructed molecular clones of the virus in the laboratory to see if the domination of the double-PTAP strains could be recreated in laboratory conditions.

“In a competition between the two viral strains under the laboratory conditions, the domination of double-PTAP viral strain was reproducible,” says Ranga. That suggests these strains may spread in the population in large numbers in the coming years.

These new variants arise from existing natural viruses through sequence duplication, he adds. But once they are made, they completely take over the job of destroying the immune system from the natural virus.

“This work, for the first time, showed that the length of sequence duplicated is greater than for the other dominant clade, clade B,” said Vinayaka R. Prasad, a professor at the department of microbiology and immunology, Albert Einstein College of Medicine, New York. He was not involved in the study.

The study also provides, for the first time, a mechanistic explanation for why PTAP duplications matter. They enable the virus to better egress from infected cells, according to Prasad.

“This paper makes a solid new contribution to our understanding of the evolution of HIV-1 C, which appears to be constantly undergoing changes and is setting itself as being very different from all other HIV-1 clades,” he added. “This may make the control of HIV-1C somewhat difficult, but this is yet to be proven.”

Challenges to the study

People in the world’s industrialised countries are affected by viruses of the HIV-1B family and all their laboratories work on that family. This way, its PTAP-variant viral strains were known decades ago.

Although Ranga’s team had an inkling about PTAP-duplicated HIV strains in India five or six years ago, he still had to test it. The study was an international collaboration between a few Indian and South African laboratories from March 2011 to March 2015. When their initial analyses found the presence of PTAP duplication in some viral strains, the researchers decided to undertake a proper study.

To get good quality clinical samples, Ranga and his colleagues collaborated with an NGO called YRG CARE in Chennai. However, limited funds for academic research (albeit from multiple governmental agencies and departments) and lack of personnel with specialised skills like next-generation sequencing, flow-sorting and mass spectroscopy proved troublesome. So they joined hands with American collaborators and sent a PhD student to their laboratory to perform some advanced experimental work.

The most concerted efforts in HIV research around the world today are focused on HIV latency. After the virus infects the cells, it actively proliferates in some of them, setting about making daughter virus particles. In some other cells, at the same time, the virus remains dormant.

This silence is called transcriptional silence or, more popularly, HIV latency.

Ranga says that the powerful anti-retroviral medicines (ARM) can kill and remove all actively proliferating HIV from the body, but they cannot do so with the silent virus. Although this as a strategy all pathogenic organisms use to beat the immune system, HIV takes this molecular trick to the next level: by being active in some cells and silent in others at the same time. The active virus exposes the system to chronic and systemic immune activations even under successful ARM therapy.

“The systemic activation leads to rapid deterioration of the immune system. On the other hand, the silent virus becomes a technical hurdle for viral eradication.”

Antiretroviral therapy (ART) can kill the actively proliferating HIV, but not the silent HIV. And until the silent virus is removed, medicines, vaccines or any other disease management strategy will but fail.

“It is like a live bomb at home that can explode anytime,” Ranga says. “Worse, we don’t even know where the bomb is hiding in the body. We only know that there is a bomb.”

Many laboratories worldwide are engaged in developing medicines to activate the silent virus and then kill it using ART, a strategy popularly called ‘kick and kill’. The future of HIV research, therefore, is focused on reversing HIV latency – to awaken the ‘sleeping’ virus. Ranga’s lab also has active research programmes in this area.

PTAP duplication and ART

Although the study does not directly affect current treatment policies, it is likely to have a strong influence in the future. The present disease management principle is to simply control the spread of the virus; there is no cure as such.

But the great thing about the extant treatment policy – ‘test and treat’, giving antiretroviral medicines to anyone as soon as they are diagnosed to be HIV seropositive – is that an HIV infection has become virtually reclassified as a chronic disease instead of being the definite death-sentence it once was. Major awareness campaigns, mandatory tests for HIV-1 and free distribution of antiretroviral drugs helped achieve this milestone.

However, the downside is the risk of the viruses developing resistance to certain drugs and enhanced recombination, especially if people are complacent about undergoing ART every day.

But Ranga says that the problem of drug resistance in HIV is not as severe as in the case of tuberculosis (TB) for technical reasons. Compared to that of the TB bacterium, The HIV genome is much smaller than that of the TB bacterium. Thus, HIV can’t afford to have a mutated genome too long, and the virus attempts to return to the original shape when a new subject is infected. So HIV tries to remain in a drug-free zone and without a need to develop drug resistance, he explains.

However, if a population is exposed to ART much earlier and for a prolonged duration, this might change. “We have to keep our eyes open to see if HIV will pull more molecular tricks [from inside] its sleeves, such as generating more recombinant forms, creating more variant forms characterised by newer molecular properties, etc.,” Ranga says.

Despite decline, 5,008 HIV cases detected last year in Karnataka

BENGALURU: Karnataka has 2.47 lakh HIV patients, the fifth highest in the country, out of which only 1.5 lakh are receiving life-saving anti-retroviral therapy (ART).

Out of 1,951 pregnant women living with HIV only 1,421 receive this treatment. Recent advances in vaccines, early treatment, cure research, diagnostics and future drugs are being discussed at the National AIDS Conference being held here from Friday to Sunday. Among those being researched are injectables to avoid taking pills everyday and implants under the skin.

Dr G D Ravindran, Professor of Medicine, St John’s Research Institute, said, “In 2017, Karnataka had 2,47,413 HIV patients, of which 1,23,821 were women. Among them 1,55,411 (62.8%) were receiving ART. AIDS-related deaths have declined in Karnataka by 68% between 2010-2017 to 8,450. Despite a 46% decline in HIV infections in the state, we still saw 5,008 fresh HIV infections in 2017.”

Dr Glory Alexander, Director, ASHA Foundation that works for HIV patients, said, “Regarding the prevention of parent to child transmission of HIV, out of the estimated 22,677 pregnant women living with HIV in India in 2017, only 13,716 of them were receiving ART which covers only 60%. However, in Karnataka, in 2017, around 70% women were covered. 1,421 women were covered against the need of 1,951. India aims to eliminate HIV transmission from parent to child. We need to be surveillant of HIV in pregnant women to ensure we do not reverse the progress made so far.”

Need for more viral load testing machines
The World Health Organization and the National AIDS Control Organisation guidelines recommend routine viral load monitoring every six months, 12 months and then every 12 months thereafter if the patient is stable on ART. Scientific evidence has shown that if every HIV patient who is on ART has an undetectable viral load, his/her risk of transmitting HIV becomes negligible. However, viral load testing in India is done only at 10 national reference laboratories for suspected cases of treatment failure.  With the number of VLTs being so low, it is not known how many of 11.81 lakh people on ART are virally suppressed.