Thursday, January 16, 2014

TAMING THE HIV SCOURGE

IN 2003, a new human immunodeficiency virus (HIV) case turned up every two days in the Philippines. By 2013, health records show there were 16 new cases that turned up each day; in October 2013, for example, 491 cases were recorded in 31 days. HIV infection that triggered after eight or 10 years the lethal acquired immune deficiency syndrome or AIDS had turned into a runaway epidemic— within the span of a decade beginning 2001, numbers of the newly HIV-afflicted declined by 20 percent while deaths tapered beginning 2005 to 24 percent across the globe.

The numbers of the afflicted climbed sky-high in the Philippines to 1250 percent.

Unfazed by such staggering figures, Dr. Edsel Maurice T. Salvaña maintains that the increase may be attributed to “(greater) awareness in the community of men who have sex with men” likely to have themselves go through medical check-ups rather than suffer in silence. Results from such check-ups find their way into health records that are collated nationwide.

In his 2013 paper, “The Changing Molecular Epidemiology of HIV in the Philippines,” Dr. Salvaña who heads the country’s Institute of Molecular Biology and Biotechnology points to a Philippine HIV epidemic but asserts HIV is “no longer a death sentence, and early detection saves lives.”

Too, “treatment can restore life expectancy and interrupt transmission.”

While effective control of the global AIDS plague remains elusive to this day, Dr. Salvaña considers HIV more of a chronic disease “after an unprecedented global effort in research and aid (that led to discovery of) effective medication. The turning point came with discovery of protease inhibitors and use of HAART—highly active antiretroviral therapy.”

Similar in appearance to a gladiator’s weapon of mayhem—a metal ball of spikes—or the burst of sun in the bloom of the shy but thorny plant makahiya (Mimosa pudica), the HIV virus can take on multiple forms, and lethal efficacy. HIV has capability to fuse with the host-cell genome—cells that survive are permanently infected. Too, the virus can mutate and thus evade host immune system. The mutation “results in a viral diversity (within the HIV type) and its rapid adaptation, in response to both immune activity and antiretroviral therapy.”

HIV can be tough to decimate or control owing to its remarkable capacity to survive—it has even shred to tatters the old-fangled classification of life forms, “millions of variants are produced within any infected person per day… recombination can lead to further diversity.” Dr. Salvaña remains optimistic though that such “viral diversity has implications for possible differential rates of disease progression, response to antiretroviral therapy (including the development of resistance), and vaccine development.”

He points to 43 circulating recombinant forms spreading in a population—CRF01_AE and CRFFO2_AG—“found principally in Southeast Asia and West Africa, respectively, while other CRFs have more limited distributions.

“Advances in full-genome sequencing of HIV have led to the identification of circulating and unique recombinant forms. Viral subtypes in a dually infected person can recombine, the recombinant form (may then be) passed to other people. CRFs are classified as such if they are identified in three or more people with no direct epidemiologic linkage, otherwise they are described as unique recombinant forms.

“Differential characteristics of viral subtypes and their interactions with the human host may influence HIV transmission and disease progression. (For instance, there is) some evidence that subtype C was transmitted more frequently than subtype B in mother-to-child transmission. Pregnant women in Kenya infected with subtype C were more likely than those infected with subtype A or D to shed HIV-1-infected vaginal cells,” he notes.

Between 1986 and 2000, Kenya did not record an increase in the prevalence of subtype C; instead an increase in the number of recombinant viruses turned up, he adds.

CRF subtype C occurs in India, Eastern and Southern Africa and represents nearly 50 percent of the global prevalence while CRF01_AE in Southeast Asia counts for 4.7 percent prevalence in a worldwide scale.

However, he cites “a survival study of 836 Thai heterosexual men and women infected with CRF01_AE showed a shorter time from HIV-1 infection to death than among those in Western populations (while a) cohort of 1,045 Ugandans did show a faster progression to death among people infected with subtype D than among those infected with subtype A.

Only 12 percent of global infections are caused by the most studied subtype B; and 50 percent of prevalent infections and 47 percent of new HIV-1 infections are with subtype C. Certain subtypes might spread or progress more rapidly than others, making treatment decisions more challenging. (Too,) data on baseline antiretroviral susceptibility derived from studies of subtype B may not be applicable to non-B subtypes,” he notes.

A 1998 paper on molecular epidemiology of HIV virus was gleaned from 54 case samples from 1985 to 1997—33 women, 21 men that include commercial sex workers, overseas contract workers and men who have sex with men— where 70% of the infections were of the subtype B.  By 1997, 29% of the cases were infected by the CRFO1_AE subtype.

Gleaning from that paper, Dr. Salvaña notes that since CRF01_AE emergence in the 1990s, the subtype occurred in three of every five (60 percent) commercial sex workers diagnosed after 1992. Too, a “shift occurred in parallel from the US military bases to the Philippine national capital region.” Simply, Metro Manila is emerging as a hotspot for the ailment.

However, of the 100 samples pooled from 1985 to 2000, 71 cases had the B subtype, 20 carried CRF01_AE, and 9 bore other subtypes. A 2013 paper based on 163 samples from 2007-2012 showed 88 (54%) were B subtype carriers, 60 (37%) with CRF01_AE, and 15 with other subtypes. Interestingly, 90 percent of samples from intravenous drug users had the B subtype. Of the 63 samples that engaged in male-to-male sex, 17 (27%) were afflicted with B, 40 (63.5%) had the CRF01_AE, and six (9.5%) bore other subtypes.

He has collated new data from which “first local evidence of lower counts of CD4 (a type of white blood cell that fights infection, their count indicates the stage of HIV or AIDS in a patient) at presentation in CRF01_AE compared to B confirms previous observations in other countries, and may be responsible for explosive increase in cases.”

Dr. Salvaña has yet to release his team’s findings: “Further analysis of data ongoing, along with transmitted drug resistance will hopefully give further insights into stopping our epidemic.”

Philippines is facing an HIV epidemic but he assures the afflicted, “it is no longer a death sentence, early detection saves lives.”

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