MP makes Com­mons his­tory with HIV speech

The dis­ease has killed mil­lions of peo­ple and is la­tent in mil­lions more. But a break­through may be near

The Guardian Weekly - - Global Report - By Jack Flana­gan

Labour MP Lloyd Rus­sell-Moyle used a de­bate in the House of Com­mons to an­nounce he is HIV pos­i­tive, mak­ing a speech he said was in­tended to tackle the stigma still as­so­ci­ated with the con­di­tion.

He is the first par­lia­men­tar­ian to make such an an­nounce­ment in the Com­mons, and the sec­ond MP to an­nounce they are HIV pos­i­tive. “I wanted to be able to stand here in this place and say to those who are liv­ing with HIV that their sta­tus does not de­fine them,” Rus­sell-Moyle, 32, the MP for Brighton Kemp­town since 2017, said in a speech that drew tributes from many other MPs.

More than 50 years af­ter it jumped the species bar­rier and be­came one of the most dev­as­tat­ing viruses to af­fect hu­mankind, HIV re­mains a stub­born ad­ver­sary. Treat­ment has im­proved dra­mat­i­cally over the past 20 years, but peo­ple who are in­fected will re­main so for the rest of their lives, and must take one pill daily – at one time it was a cock­tail of 30.

But now, as an­other World Aids Day has passed, sci­en­tists are be­gin­ning to ask if the big­gest break­through – an out-and-out cure for the tens of mil­lions who have con­tracted the virus – could be in sight.

The ex­cite­ment lies in re­search that is hav­ing some suc­cess in draw­ing the virus out of a la­tent stage so that it could be de­stroyed.

“The last cou­ple of years have been very ex­cit­ing on this front,” said Satish Pil­lai, an associate pro­fes­sor in HIV re­search from the Univer­sity of Cal­i­for­nia, San Fran­cisco. “We’re now at­tempt­ing find the holy grail of HIV re­search.”

“In the first in­stance, we want to iden­tify the sig­na­ture char­ac­ter­is­tics, in a re­li­able and ac­cu­rate way, of la­tently in­fected cells,” Pil­lai said, speak­ing of HIV-in­fected cells that evade cur­rent treat­ments.

“The other side is that we’re de­vel­op­ing novel strate­gies to de­stroy them once we’re able to iden­tify them.” We’re en­ter­ing this new era of find­ing a func­tional cure to erad­i­cate the virus,’ he ex­plains.

The dif­fi­culty be­hind cre­at­ing a cure for HIV is that, un­like other viruses, HIV-in­fected cells are able to “hide” by en­ter­ing a rest­ing phase that makes them in­vis­i­ble to our im­mune sys­tem and cur­rent treat­ment ther­a­pies.

These “la­tently in­fected” cells then ex­ist in reser­voirs in the bod­ies of those with the virus, and can launch new, re­sis­tant at­tacks if treat­ment is dis­con­tin­ued.

In last few years, sci­en­tists have found that de­stroy­ing this last reser­voir of cells will be the fu­ture of a cure.

“Peo­ple have been look­ing into la­tency long be­fore this be­came a fo­cus for a cure,” said Dr Jonathan An­gel, chief of the Di­vi­sion of In­fec­tious Dis­eases at Ot­tawa Hos­pi­tal Re­search In­sti­tute. “There have been peo­ple work­ing on HIV re­search for a long time, but only re­cently has the tone shifted.

“In my per­sonal opin­ion, our ther­a­pies have be­come so good that look­ing at bet­ter ther­a­pies has be­came fu­tile. Peo­ple are tak­ing a pill once a day with no side af­fects. That’s hard to im­prove upon.”

In fact, the in­creased ef­fi­cacy of an­tiretro­vi­rals has curbed the dead­li­ness of the dis­ease sig­nif­i­cantly. The virus ex­ists in around 36.7 mil­lion peo­ple around the world and, although it killed around 1 mil­lion peo­ple in 2017 ac­cord­ing to UNAids, that rep­re­sents a drop of al­most 50% from 2005, when mor­tal­ity from Aids-re­lated ill­nesses was at its peak.

This drop is due to im­proved medicine, as well as lo­gis­tics and pa­tient aware­ness. But the virus re­mains a grave health prob­lem in ru­ral ar­eas that lack these re­sources, es­pe­cially in re­gions such as Africa – over a quar­ter of peo­ple in Swazi­land have the virus.

The con­tin­u­ing dead­li­ness of the dis­ease in some re­gions, the tremen­dous ex­pense and pres­sure on pa­tients, means that a cure is nec­es­sary. There are a num­ber of dif­fer­ent ap­proaches cur­rently be­ing stud­ied.

One ap­proach, of­ten named the “kick and kill” or “shock and kill”, aims to kick the rest­ing cells out of their sleep so they can be pin­pointed and elim­i­nated.

Sarah Fidler, pro­fes­sor of HIV medicine at Im­pe­rial Col­lege Lon­don, who re­cently led a ma­jor study test­ing the ef­fi­cacy of the kick-and-kill method said: “The idea is to re­ac­ti­vate the la­tent cells, so they start pro­duc­ing the pro­teins on their sur­face so they look dif­fer­ent from healthy cells. We would do this with some kind of drug, which is what we’re in the process of de­ter­min­ing.”

The other re­search ap­proach wants to find and de­stroy the HIV-in­fected ‘While sci­en­tists might con­sider this a cure, the gen­eral pub­lic might not’ cells while they’re still in the rest­ing state. The key to do­ing this would be find­ing some­thing dis­tinct about an in­fected, rest­ing cell – as op­posed to a healthy one – so that an an­tivi­ral agent can tar­get them. Sci­en­tists call this elu­sive tar­get a biomarker.

There is promis­ing work be­ing done with an­tivi­ral-viruses – viruses that are en­gi­neered to tar­get and de­stroy other viruses. A spe­cific strain, the rhab­dovirus called Maraba virus (MG1), has been en­gi­neered to seek out faulty cell com­mu­ni­ca­tion, some­thing that hap­pens in both cancer and HIV. A dif­fer­ence as small as this, be­tween healthy and un­healthy cells, is enough for some­thing like MG1 to tar­get.

An­gel says the MG1 ap­proach only oc­curred be­cause of the phys­i­cal prox­im­ity of sci­en­tists re­search­ing cancer and HIV.

“The MG1 project came up on the side from be­ing on the same floor as on­col­ogy, and see­ing sem­i­nars from guys in cancer re­search,” An­gel said. “There are viruses that are able to kill cancer cells based on the fact that they have im­paired in­ter­feron sig­nalling [pro­teins made by cells to pre­vent virus repli­ca­tion]. This is an in­nate an­tivi­ral mol­e­cule, present in all of our cells to ward off viruses.

“We know that HIV can in­ter­fere with those path­ways, but what is not known is whether that is the case with la­tently in­fected cells, be­cause they oc­cur with such a low fre­quency in the body.

“MG1 as a po­ten­tial ther­a­peu­tic agent that can ex­ploit these cells.”

Although there is con­sen­sus that de­stroy­ing the virus reser­voirs is the next step, there are dis­agree­ments about whether this could be called a cure, as we un­der­stand the term.

“Com­pletely elim­i­nat­ing the reser­voirs of HIV would re­sult in a cure. The dis­sen­sion might ex­ist on what is re­ferred to as a ‘func­tional cure’,” An­gel said.

“This refers to es­tab­lish­ing a state where the im­mune sys­tem it­self (with­out an­tiretro­vi­ral ther­apy) can con­trol the virus so it is not de­tectable in the blood and there is no ef­fect on the im­mune sys­tem.

“While the sci­en­tific com­mu­nity might con­sider this a cure, the gen­eral pub­lic might not,” he said.

The speed of the re­search has been made pos­si­ble be­cause of the com­mu­nity that stands be­hind it, says Fidler. “We are talk­ing about a com­mu­nity of peo­ple with HIV that have been an ex­tra­or­di­nary driver in re­search­ing the con­di­tion,” she said. “In our most re­cent trial, no one dropped out, which is prac­ti­cally un­heard of.”

“It’s still a very stig­ma­tis­ing con­di­tion. Peo­ple don’t feel com­fort­able with talk­ing about it, as they might with di­a­betes or cancer,” Fidler said.

“I think it mo­ti­vates this col­lab­o­ra­tion. Peo­ple still feel that they are some­how dif­fer­ent and that’s what makes peo­ple join to­gether, they re­late to these other peo­ple who have the virus. They are a po­tent ad­vo­cacy force.”


50 per cent The drop in deaths from Aids-re­lated ill­nesses from a 2005 peak


A Jor­da­nian cit­i­zen with HIV cov­ers his face to hide his iden­tity


A young HIV­pos­i­tive mother on an­tiretro­vi­ral ther­apy in Malawi

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