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Weekly Bulletin

Edition 33: 18th - 24th August 2019 
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Kenya Health Summit 2019 leaves CSOs and Communities questions on UHC Unanswered!

 
       
 CS Sicily Kariuki and high-level MoH team at the Kenya Health Forum last week                                              

The National Health Summit closed in Nairobi last week leaving civil society organizations, including networks of people affected with the diseases with more questions with regard to the roll-out of universal health coverage in Kenya. Under the theme, ‘Partnering for UHC: Delivering affordable quality healthcare for all’, the Kenya Health Summit was convened by the Ministry of Health to secure commitments from stakeholders to take definitive action towards transforming the health sector.  Coming one year after the launch of the UHC pilots in 4 counties, the 2019 Kenya Health Summit was expected to provide clarity with regard to the progress and status of the roll-out of universal health coverage in Kenya. And when it closed last week, no clarity in terms of progress and status of UHC was shared leaving CSOs and communities with their questions unanswered and their anxieties un-addressed. 

The UHC pilot in the 4 counties: Kisumu; Nyeri; Machakos and Isiolo is the initial part of a grand scheme aimed at rolling out universal health coverage in Kenya. The focus on UHC intensified after President Uhuru included health for all as part of his Big 4 Agenda. The President’s Big 4 Agenda that includes access to quality health care for all Kenyans is now touted as part of the President’s legacy. If delivered, universal health coverage will be one of the rare cases where promises by the political leadership come to be true. During his inauguration for the 2nd term, President Uhuru Kenyatta promised “
100% access to universal health coverage to all Kenyans”. It is this promise that the CSOs have been paying attention to. So far, there is not a single indication that this promise will be delivered by 2022.

Before the National Health Summit could close, a section of the delegates from the four UHC pilot counties had stated grumbling and questioning the commitment by the national government to the delivery of UHC goals. According to these delegates, the national government officials are not keen with the achievements of the UHC and in fact the real obstacles to improving the health and well-being of communities. This assertion was later during the weekend confirmed by a section of the media by asserting that: “the government is yet to release Sh951 million to procure drugs and non-pharmaceutical supplies for the 3rd quarter of universal health coverage”. Under the UHC pilot, a significant allocation (70%) was to be managed by the Kenya Medical Supplies Agency (KEMSA) for the procurement of the drugs and non-pharmaceutical supplies.

Delays in monies aside, the CSOs had hoped that the National Health Summit would provide an opportunity for the interrogation of the progress and status of the UHC pilots. It was also hoped that the Ministry of Health leadership would shed light on the plans for the roll-out of the UHC pilots. These two key areas were not tackled. No concrete result was shared and no plans were presented. With no status and progress update, it was not possible to deliberate on the next steps after the UHC pilots. This too has been a concern by the CSOs and community’s leadership.  And when the Summit focused on the everyday talk on how to improve the health and wellbeing of Kenyans, the disappointment on the faces and minds of CSOs and communities was not surprising. 

 

Why this team of Adolescents and Young People are committed to Annual Paintings.

Sample drawing by the younger Adolescents last week
 
Last week, representatives and adolescents and young people converged at the NEPHAK Nairobi offices for what has now become an annual painting event. As we reported in this Bulletin last year, the painting for and with young girls was introduced to NEPHAK by Gelise McOllough who ventured into part-time painting for education to support young girls living with HIV to enroll and stay in schools. With time, this venture proved beneficial to those who venture into it in many ways. The paining exercise also gives girls and their parents/guardians what to do in their spare time. The painting for education is now an annual event. See the past issue of the NEPHAK Bulletin: http://mailchi.mp/5c13e2b3ecca/nephak-weekly-bulletin-issue-34. For more about the work of Gelise, see: http://www.gelise.org

As we shared before, the painting for girls’ education is informed by the fact that young women and adolescent girls are at increased sexual health risks, including HIV and are more likely to drop out of schools. The prevailing social norms and cultural beliefs make parents reluctant to fight for girls’ education. The reluctance is very real when an adolescent girl or young woman is infected with HIV. In Kenya, this is also due to the fact that most of the young people born and living with HIV have lost one or both parents. Orphans living with HIV are more likely to drop out of education. Therefore, Gelise has been painting with girls and then helping them to sell some of the paintings and the proceeds that come from the sale is plowed into the girls’ education. In this way, Gelise enables young girls to stay away from the sexual health risks that face young girls and keep them out of school. 

There is another reason behind the annual painting event by the NEPHAK. It is an opportunity to catch up with the young girls, some of them in boarding schools. For those who care, Kenya is set to deliver on its 90.90.90 targets by the set date of next year. Not for children. Not for adolescents (11 – 19 years) and not for young people (20 – 24 years). Latest data confirm that adolescents (11 – 19 years) and young people (20 – 24 years) continue to be left behind as the country counties to make progress towards the delivery of the 90.90.90 targets. The challenge is in achieving and sustaining viral suppression especially for learners living with HIV. The situation is really bad for young learners living with HIV. Clearly, learning institutions will still need to do significant adjustments to become friendly to HIV positive learners.

However, for young people, the annual painting event is not just for catching up. It is important for them because some of them managed to go through schooling through the support of the painting for education. Even more important for those who are in schools through the same support. And while catching up with friends is a significant part of the painting, the young people are in it because of the hope and opportunity it provides. The hope and opportunity to stay in school and start to think about the future. NEPHAK is committing to this annual event to stay in solidarity with the children. 

 

Could a better understanding of inflammation help research towards an HIV cure? 

 
Although we already shared with the NEPHAK membership and the Kenya PLHIV community the relevant summary learning from the 10th International AIDS Society Conference on HIV Science (IAS 2019) that happened in Mexico City last month, we have also come across an additional piece that should inspire the Bulletin’s readership. This is related to the immune activation and HIV-induced inflammation and which can be found here: https://www.aidsmap.com/news/jul-2019/could-better-understanding-inflammation-help-research-towards-hiv-cure?utm_source=NAM-Email-Promotion&utm_medium=aidsmap-news&utm_campaign=aidsmap-news 

We should all be informed that low-level HIV inflammation generally persists in individuals, even when their HIV viral load is well controlled (undetectable) by antiretroviral therapy (ART). This inflammation occurs in most people with HIV who started ART at the chronic stage of their infection (i.e. after primary infection). A well-known consequence of HIV-associated chronic inflammation is the increased risk of non-AIDS related co-morbidities (such as cardiovascular disease and cancers) and mortality.

During primary HIV infection, prior to ART, the level of inflammation is very high and is a strong predictor of HIV disease progression. Therefore, studies have shown that the earlier ART is initiated during the acute phase, the better. Benefits include decreases in the size of the HIV reservoir, in viral diversity, in immune activation, and in inflammation; as well as faster immune restoration.

However, scientists had hoped that starting ART in the very early days of acute infection would normalize levels of T-cell activation and inflammation. Unfortunately, in several studies, inflammation markers have not shown this outcome, even long after ART initiation. One example comes from the Thai cohort of acute HIV infection, where levels of TH17 cell (a type of CD4 T-cell producing Interleukin-17) in the gut did not return to normal after a long period on ART.

So, how might chronic inflammation contribute, even under long-term ART, to the establishment of the HIV reservoir? Many studies have addressed this question, suggesting several mechanisms. Chemokines (small proteins secreted by cells to mobilise and activate infection-fighting white blood cells, that are involved in many immune and inflammatory responses), for example, are known to rise after HIV infection and might be responsible for attracting new target cells – in particular, activated CD4 T-cells – to infected tissues, where they will be infected and fuel viral replication. Chemokines also have the capacity to enhance latent cells or viral replication, as demonstrated in several studies.

In the meantime, chronic inflammation can impair immune responses in several ways. For example, inflammation increases levels of PD-1 receptors, known to dampen the functionality of T-cells that are faced with repeated stimulation from chronic infections or tumours. Eventually, inflammation causes damage to the gut and lymphoid tissue, additional to that which occurred during acute infection.

Müller-Trutwin briefly reviewed the many studies that have tested or are testing medications, sometimes from other disease fields, against HIV-induced inflammation. They range from cytokine inhibitors and valganciclovir (an anti-CMV drug) to statins (cardiovascular drugs, now known to also reduce inflammation), to a combination of vitamin D and exercise. So far, most have had inconclusive results.
There is still a need to understand why HIV induces inflammation, even when the viral load is undetectable, and to determine what mechanisms might be able to regulate the phenomenon.

In this field, researchers can learn a lot from non-human primate models. Once they are infected with SIV (Simian Immunodeficiency Virus), Asian macaques progress to AIDS in a similar way to humans with HIV (this is why they are called ‘pathogenic models’). On the other hand, African green monkeys and sooty mangabeys are ‘natural hosts’. Despite having high levels of viraemia in their plasma and their gut, as humans do, they don’t have chronic inflammation.

How do they escape inflammation? This is still unclear. But we do know that these natural hosts do not lose TH17 cells; they maintain their intestinal barrier; they do not show bacterial translocation (the passage of bacteria from the gastrointestinal tract to other organs, through the intestinal mucosal barrier, when it becomes permeable due to inflammation); and their lymph nodes are not destroyed. As a matter of fact, while the African primates do not generally control viral replication, they do so very strongly in their lymph nodes. One probable cause of this very localised and efficient control of viral replication is the migration of natural killer (NK) cells (cells in the immune system which attack and destroy infected cells or tumour cells) into the lymph nodes.

This raises an obvious question: why are these natural hosts capable of locally controlling viral replication, and why does this not happen in the Asian macaques? Müller-Trutwin presented preliminary data from an ongoing examination of NK cells in African green monkeys (natural hosts), showing an expansion of NK cells. This is distinct from the processes in Asian macaques following SIV infection. The notion of a differentiation of NK cells is a new discovery. “You knew about it for T-cells, not for NK-cells,” she said.
Building on this finding and the role of IL-21, a cytokine without which the differentiation of NK cells cannot happen, Müller-Trutwin’s team have joined an existing study on ART in Asian macaques infected with SIV to observe NK cells and see what happens if IL-21 is combined with ART. The study has two arms, each with eight macaques, receiving either ARTand IL-21, or ART alone.

NK cells from the treated macaques were analysed at several time points. Following the first round of IL-21, NK cells started to show suppressive activity against viral replication. Greater suppression in comparison with the other arm was clearly confirmed after the second round, and more results are promised in the future. In her conclusion, Müller-Trutwin highlighted again that more biomarkers of tissue damage and repair were needed to monitor interventions; that the lead of NK cells was definitely worth pursuing, as they might play a key role in the reduction of the HIV reservoir; and that many lessons can be learnt from natural hosts, on the path towards an HIV cure.
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NEPHAK Weekly Bulletin is published by the Advocacy and Communications Office at the NEPHAK National Secretariat. Articles can be reproduced freely as long as NEPHAK is acknowledged. Further details can be obtained from The Editor Tel: 0720209694, Email:info@nephak.or.ke, Website: www.nephak.or.ke, Tweet us: @NEPHAKKENYA

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