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Nearly everything is right about the Conference on Retroviruses and Opportunistic Infections (CROI) except the official color. AdvertisementThe 12th CROI, held February 22-25, 2005, in Boston, paid special attention to prevention of mother-to-child transmission with that embattled nonnucleoside reverse transcriptase inhibitor (NNRTI), nevirapine (NVP). In the archives of antiretroviral hagiography, no story has more deaths and resurrections than NVP's. In a perspicacious and palliative talk, James McIntyre (Chris Hani Baragwanath Hospital, Johannesburg) observed that a solitary dose of NVP does not cause liver failure [abstract 8].
The tragedy is not that so many pregnant women are taking this drug, McIntyre counseled, but that so few do. But a sole dose of NVP does breed resistant virus -- probably in every infected woman who takes it. With Johannesburg colleagues, Jeffrey Johnson (US Centers for Disease Control and Prevention [CDC], Atlanta) deployed a real-time polymerase chain reaction (PCR) assay trained to ferret out the K103N NNRTI resistance mutation in subtype C virus, the prevalent subtype in a South African study of single-dose NVP [abstract 100]. Johnson focused on 50 women in whom neither standard sequencing nor real-time PCR spotted K103N before they took one dose of NVP.
Searching plasma samples collected up to nine months after single-dose NVP, even Johnson's real-time PCR test couldn't see Y181C in six samples examined at three to six months or in five samples scoured at six to nine months. Overall, Johnson figured that two thirds of women studied with real-time PCR had K103N or Y181C after single-dose NVP, a 62 percent jump from estimates with standard sequencing. Reading an allele-specific PCR meter, Sarah Palmer (National Cancer Institute, Frederick, Maryland) confirmed that K103N and Y181C hang on for months after solo-dose NVP, even if routine sequencing can't spot them [abstract 101].
In Palmer's study the overall frequency of mutant virus, 69 percent, equaled the rate figured by Johnson.
If even these supersnooping assays see resistant virus in about two thirds of samples from women who take single-dose NVP, why do Richman and Clavel think virtually everyone who swallows the drug once ends up with resistant virus?
Shayne Loubser (National Institutes for Communicable Diseases, Johannesburg) used real-time PCR to trawl for mutations locked up in viral DNA inside peripheral blood mononuclear cells (PBMCs) [abstract 102].
Arguments over persistence of NNRTI-resistant virus boil down to one burning question: What does this resistance mean clinically? Another clinically crucial question is how well NVP will prevent HIV transmission when women try the single-dose regimen a second time. This prospective study involved women taking NVP to avert transmission in a second pregnancy.
Another clinical concern arose in a study of infants taking NVP or lamivudine (3TC) monotherapy to ward off HIV in breast milk [abstract 93].
Giuliano urged wider use of rapid HIV assays after birth to avoid exposing infected infants to prophylactic monotherapy. At best, most resistance studies show that one mutation or another provoked by drug A but not drug B leads to faster virologic failure.
A multivariate model of baseline and time-dependent factors rounded up some familiar suspects in shortened survival -- older age, less physician experience with HIV, worse adherence, lower baseline CD4 count, and higher baseline viral load. Hogg and resistance maven Richard Harrigan did not speculate on why failure of NNRTIs -- but not PIs -- ups the odds of death. As one structured treatment interruption (STI) stratagem after another falls on barren ground (see "Two more dead-end STI salvage studies" on page 74 of the March 2005 issue of the IAPAC Monthly), CD4-guided drug breaks remain a tempting (though possibly beguiling) option for people longing to shorten their time on treatment. Even nine months of freedom from antiretrovirals probably sounds like a good deal to lots of people. Looking for resistance mutations during and after drug breaks guided by CD4 counts or viral load, Lidia Ruiz (IrsiCaixa Foundation, Barcelona) found them in 32 of 87 break takers (37 percent).
Nine of 19 people (42 percent) who suspended an NNRTI regimen ended up with nonnuke mutations. Together these studies tell a cautionary tale: Despite mostly gladsome news on CD4-guided drug breaks, these holidays can have unhappy endings.
When baseball hero and barroom sage Yogi Berra dismissed a familiar hangout with the epigram "no one goes there any more -- it's getting too popular," he might have been describing today's drug resistance patterns. Breaking isolates into six-month clusters based on 1998 to 2004 submission dates to Virco, mutation counters tallied more than 3,330 NNRTI mutation combinations not seen in earlier half-year periods, more than 17,200 NRTI mutation patterns making their debut, and more than 22,700 PI mutation arrays with no forebears in Virco's vaults. These findings should stir more than idle curiosity; they reflect the necessarily gnarled dynamics of viral evolution, as HIV beads strings of amino acid substitutions aimed to escape drug pressure and keep itself fit. Genotyping after the rebound did not turn up I50L, the signature mutation seen with failure of unboosted ATV. But don't expect top HIV clinicians to agree about genotypes, phenotypes, or both when picking rescue regimens. Zolopa dealt out GTs, PTs, and GT-PTs in random order and made sure all samples had decreased susceptibility (PT resistance) to at least one drug. Given these ground rules, the percentage of "acceptable" calls may rank as a minor miracle. Zolopa believes the results suggest that the resistance test used "may result in very different antiretroviral treatment regimens for some patients." Using PT or PT plus GT may yield better results than GT alone, he proposed. Parikh concluded that regimens including AZT and nucleosides or nucleotides that select K65R have a high genetic barrier to resistance and merit further study. After a median 48 weeks of follow-up, 19 people (88 percent) chiseled their viral load to a sub-50 sum.
But if 3TC has an edge over FTC in slamming 67-70-219 TAMs, d4T may outpunch AZT on this so-called TAM-2 pathway, according to a 625-sample analysis by Alessandro Cozzi-Lepri (Royal Free and University College Medical School, London) [abstract 708]. Even more intriguing was the suggestion that d4T-containing regimens may beat back TAM-2 virus, while AZT regimens roll over when faced with those mutations. On the lipodystrophy front, a randomized study saw benefits for TDF over ABC when swapping out a thymidine analog.
Klein ranks among the premier tollers of the MI tocsin with his early report that men with HIV landed in the hospital for heart disease much more often than men without an HIV diagnosis.7 But that early work failed to forge a significant link between PI therapy and heart problems. Aquitaine cohort researchers gauged smoking rates and PI and antilipid drug use from 2000 to 2003 to estimate their effect on carotid artery intima media thickness (IMT), a sturdy predictor of heart disease [abstract 871]. During the first year of follow-up, eight more people started fibrates, eight tried statins, 42 switched from their PI, and 10 quit smoking. Over the next two years, 52 more people abandoned PIs, 30 more started antilipid drugs, and 14 more stopped smoking. A gurgling datastream from company-sponsored ATV trials documents improved lipid profiles in people who switch from other PIs to ATV. At the 11th CROI in 2004, a 16-week trial failed to find a triglyceride advantage for fish oil (omega-3 fatty acid) plus diet and exercise counseling versus counseling alone.8 That small study used a European product called Coromega at a dose of about 3 g daily. When several studies showed that trading d4T or AZT for ABC reversed limb fat losses, ABC became the natural choice in such swaps.
Three of 52 people (6 percent) randomized to TDF quit the study before week 48, compared with eight of 53 (15 percent) assigned to ABC.
Subanalyses of 48-week DEXA results suggested that people switching from AZT did better with ABC (+210 g versus +66 g with TDF), while people taking d4T at baseline gained more with TDF (+529 g versus +375 g with ABC). A 24-week study at 15 ACTG sites found better peripheral fat gains with a non-NRTI regimen than with a simple switch of d4T or AZT to ABC [abstract 45LB].
Other studies tracked bone, glucose, and kidney complications in people taking TDF with or without ddI.
Combining TDF with 400 mg of ddI daily raised the risk of hyperglycemia in a retrospective comparison of 78 people taking both drugs, 42 taking only TDF, and 57 taking only ddI [abstract 829]. Hulgan compared 147 people who had grade 1 or worse neuropathy with 362 no-neuropathy controls.
One hesitates to add a single phoneme to the farrago surrounding the New York City man who became infected with multidrug-resistant, dual-tropic virus and crashed from party-prowling vigor to AIDS in as few as four months.
Readers with keen interest in this case surely memorized the details long ago, and this review will not add to the nimiety.
Some gay men -- some of them in the later reaches of middle age -- routinely and knowingly risk HIV infection, often while taking highly addictive crystal methamphetamine. The viral strain that infected the New York case can use either X4 or R5 coreceptors, a nimble feature that may boost the risk of rapid progression.
The progression rate in the New York case puts this man in the top 0.5 percentile of progressors in the Multicenter AIDS Cohorts Study, a cluster of gay men. Besides dual tropism, no viral or host factors yet considered explain the fast progression. Despite the multidrug resistance of this virus, it grows better than many nonmutant strains in lab dishes (see note 17). Possible susceptibility of the virus to only the fusion inhibitor enfuvirtide (ENF) and the NNRTI EFV compromises prospects for long-term control. Across North America and Europe, the HIV epidemic has become a babel of viral subtypes, ethnic helter, and social skelter -- applied in a rich schmeer of risk behaviors. Despite a big population of HIV-infected people from sub-Saharan Africa, France may be looking at a resurgent gay epidemic. These findings may mean that HIV has started spreading faster among French gays, Semaille concluded, that more gays got tested recently, or both. Gay men in France are giving each other not only HIV, but also hard-to-treat genotype 4 hepatitis C virus (HCV), reported Marie-Laure Chaix (René Descartes University, Paris) [abstract 122].
Anybody may and many do, according to the most recent six-state analysis by the CDC [abstract 674]. As Bennett noted, though, the analysis may under-represent people diagnosed in private practice or nonpublic centers. Bennett and collaborators collected 787 samples from newly diagnosed (not necessarily recently infected), untreated people and genotyped them for reverse transcriptase and major protease mutations.
A substudy of 633 demographically grouped people revealed no differences in rates of infection with resistant virus by race or ethnicity, HIV transmission group, age, or gender (Table 3). As in the six-state CDC audit, transmission of NNRTI-resistant virus is climbing in New York City. The bustling trade in NNRTI mutant virus between sex partners "necessitates caution when considering initial empiric combination therapy with NNRTIs," the Aaron Diamond team counseled. Charles Hicks (Duke University, Durham, North Carolina) looked for resistance mutations in two North Carolina groups of acutely or recently infected untreated people -- 110 referred to HIV clinics at Duke or the University of North Carolina (the "clinic" group) and 127 diagnosed at state-run HIV testing centers (the "state" group) [abstract 673]. The clinic and state groups did not differ much in age, with medians of 27 years (range 17 to 89 years) in the clinic and 30 years (range 15 to 59) in the state.
Together these two studies suggest a sadly similar rate of resistance transmission in rural and urban North Carolina and on New York's mean streets.
Soon after people first get infected with HIV, they may be particularly prone to adding a second or "super" infection, proposed Robert Grant (Gladstone Institute, San Francisco) [abstract 287].
Cody: A wild-type virus replaced multidrug-resistant HIV 43 to 53 weeks after his first infection.
If a few insights into the threats of superinfection or infection with resistant virus cannot inspire a sober regard for HIV's wrath, watching the Webcast of a CROI plenary talk by Daniel Douek (US National Institutes of Health, Bethesda) might do the trick [abstract 127, see note 18]. People who blithely risk HIV infection (and maybe even some clinicians who see them) may consider acute infection a nasty but self-limiting sweaty bout that does little immediate damage -- surely nothing that antiretrovirals can't fix five or six years down the road. The primary target of acute HIV infection is the body's total battalion of memory CD4 cells -- the very cells the body needs to counter other invaders. As many as 60 percent of memory CD4s can be infected in this acute assault.19The memory CD4 infection rate is more than 100 times higher in acute infection than in chronic infection. After 14 days of infection, 80 percent of infected memory CD4s are dead -- half of all memory CD4 T cells.
Magid Herida (Institut de Veille Sanitaire, Saint-Maurice, France) and colleagues retrospectively analyzed stored rectal specimens from January 2002 to April 2004 and prospectively rated samples from five Paris STD clinics and the national reference center in Bordeaux. Collecting epidemiologic data from the first 14 people with rectal LGV, Herida found that all were gay men reporting unprotected anal sex with pick-up partners.

Symptom duration ranged from 11 to 120 days before diagnosis (median 50 days) and included rectal pain, discharge, and tenesmus (painful spasm of the urogenital diaphragm).
From the Netherlands, Joke Spaargaren (Municipal Health Service of Amsterdam) and coworkers reported a new Chlamydia trachomatis strain causing LGV in gay men [abstract 896].
With polymerase chain reaction (PCR)-based genotyping and gene sequencing, Spaargaren learned that 39 of 51 samples from symptomatic men (78 percent) bore a new L2b strain of C. Methicillin-resistant Staphylococcus aureus (MRSA) infection crops up in children, prisoners, athletic teams, and now HIV-infected gay men. In a retrospective cohort analysis of 3,455 HIV-infected people who visited the Owen Clinic at least once between January 2000 and December 2003, Mathews cataloged 94 cases of MRSA, 38 (40 percent) defined as community acquired and 56 (60 percent) as nosocomial (probably picked up in a hospital or extended-care facility, or from an indwelling catheter).
Diagnosis of community-acquired or nosocomial MRSA jumped more than six times over the four years of study, from under one case per 100 person-years before 2003 to about five per 100 person-years in the second half of 2003.
Mathews cautioned that the climbing incidence may reflect heightened scrutiny as clinicians learn about MRSA, and unmeasured confounders like active substance abuse or short-term antibiotics could fudge the findings.
Rieg rated seven of the eight MRSAs as community acquired, because one carrier had been in the hospital in the past half year. Because few HIV-infected gays in this population carry MRSA in the nose, Rieg suggested that skin-skin or skin-fomite contact may explain transmission. The temptation to drape oneself in censorious dudgeon over the self-destructive sexploits of today's party gays is probably best stifled. But it's hard to answer Harold Jaffe's (University of Oxford, England) question about why gay men still risk their health almost 25 years after he helped us understand how HIV spreads.
For the three-year study, researchers studied more than 20,000 circumcised adult men in the South African township of Orange Farm. Scientists believe the foreskin is susceptible to tears during intercourse, allowing HIV to get into the bloodstream. Fancy living somewhere with low taxes, affordable real estate and a reasonable cost of living? Originally called the "National Conference on Human Retroviruses," CROI now hosts an international cast with a global (but strictly scientific) agenda. This second part of the IAPAC Monthly's conference coverage also probes studies on resistance during chronic infection, antiretroviral side effects (the "vexations"), and the gay epidemic in North America and Europe (the "flirtations"). The past year featured this drug's second or third crucifixion, this time for messy data handling in the landmark trial of single-dose NVP for perinatal prophylaxis -- coupled with unhappy toxicity reports.
No significant clinical or laboratory toxicities emerged in 4,429 women or 4,875 infants exposed to single-dose NVP in six trials, in addition to the much-bruited HIVNET 012. He estimated that about 3 percent of HIV-infected pregnant women who need NVP or other short-course antiretrovirals get them. That judgment came from resistance savants Douglas Richman (University of California, San Diego) and François Clavel (Bichat-Claude Bernard Hospital, Paris). The assay can dig up K103Ns comprising a mere 0.2 percent of a viral population, whereas standard nucleotide sequencing can't see virus making up less than 20 percent of a population. After treatment the standard assay sighted K103N in 10 of 50 samples, and the souped-up CDC assay confirmed that finding.
With a population detection limit of 0.3 percent, the assay saw no Y181Cs before women took NVP. But K103N touched off the real-time PCR alarm in four of six samples surveyed at three to six months and in three of five at six to nine months. Palmer's analysis involved three groups of women enrolled in NVP prophylaxis trials -- eight in whom standard sequencing saw resistant virus six weeks and six months after single-dose NVP but not at 12 months, 11 in whom the standard test registered resistant virus at six weeks but not six or 12 months, and 10 in whom standard testing eyed no mutations in the six-week sample. Because Johnson's and Palmer's PCR tests espy mutations only in plasma samples, but most virus -- resistant or otherwise -- takes cover in deeper lairs. The good news is that he graphed rapidly dwindling K103N frequencies in DNA over time, seeing almost none after 12 months. The only published study to address this question, involving Thai women taking NVP for their own health, found equivalent six-month CD4 gains in women with and without earlier exposure to the drug.1 But women who took one NVP dose earlier had a worse six-month virologic response than those starting the NNRTI for the first time, and women with genotypic evidence of resistance to NVP did even worse. A case-control study by Neil Martinson (Johns Hopkins University, Baltimore) tried to find an answer, but his conclusion did not satisfy everyone [abstract 103].
Dissenters argued that the wide confidence interval may not mean repeat NVP works as well as first-time NVP, but that the study lacked statistical power to discern a clear difference. The resistance risk proved particularly high in 26 neonates studied by Marina Giuliano (Istituto Superiore di Sanità, Rome) because they all picked up HIV at birth or shortly afterwards, though the virus went undetected at the time. A cross-border collaboration between clinicians in Orléans, France, and Madrid confirmed earlier reports that people with lower CD4 nadirs have to restart antiretrovirals faster during CD4-guided breaks [abstract 585].
But besides the risk of retinitis and other ugly setbacks, everyone should know that resistance also poses a threat during CD4-steered STIs. Among the 31 people with NRTI-linked mutations, 25 had sampled NRTI monotherapy or duo-therapy before taking a stronger combo, and most of them had thymidine analog mutations (TAMs) reflecting this earlier treatment. In seven of these nine the mutations arose during the drug break, and in two after they resumed treatment. In a review talk at CROI, Diane Havlir (University of California, San Francisco) -- no milquetoast when it comes to novel strategies -- warned that CD4-guided breaks still need rigorous study to sort out their risks and benefits [abstract 181]. Elbowing his way through a crowd of 128,456 viral isolates on tap at Virco, Alex Rinehart discovered that the "most common" mutation combinations are turning up less and less [abstract 684].
At the same time, 97 percent of PI mutation sets, 95 percent of NRTI mutation sets, and 87 percent of NNRTI mutation sets showed up in 10 or fewer isolates. While Virco's Rinehart offered a satellite-high view of that breakneck evolution, Eoin Coakley (ViroLogic) snapped a submicroscopic close-up of a unique mutation tweak in one individual [abstract 716]. But N88S, encountered in vitro but never apart from I50L in clinical isolates, did appear (along with some minor protease changes).
That conclusion emerged from a crafty exercise cooked up by Andrew Zolopa (Stanford University, California) with help from Stephen Becker (Pacific Horizon Medical Group, San Francisco), and some ViroLogic stalwarts [abstract 727].
Otherwise the samples could have no, minimal, moderate, or significant PT-GT discordance, resensitization or hypersusceptibility to certain drugs, quantifiable differences in PT susceptibility without PT-GT discordance, or PT-GT discordance attributed to mixtures in genotype.
The median percentage of regimens with at least three "acceptable" drugs was 65 percent (range 37 percent to 96 percent) for interpreting GTs, 86 percent (range 42 percent to 99 percent) for reading PTs, and 86 percent (47 percent to 97 percent) for PT plus GT.
But he cautioned that this study cannot clinch that conclusion because it did not factor in actual outcomes in the people whose virus got analyzed.
Even when they deign to share the same viral population, they almost never show up on the same genome, according to a detailed study by Urvi Parikh (University of Pittsburgh) [abstract 98].
French clinicians reported four virologic failures and five toxicity dropouts among 42 people who took the regimen for eight months [abstract 599]. Most of 22 people who picked up K65R with or without M184V returned to the realm of undetectability after 14 to 177 weeks of rescue therapy. Among the three people who did not, two earned a "lost-to-follow-up" label and one had adherence problems.
Early results from 3TC's maker, Glaxo, suggest these mutants may stay susceptible to 3TC more often than to FTC, though the differences in many cases were slim [abstract 713]. Although a cohort study logged signs of kidney problems with TDF, the clinical significance of those hints (if any) remains obscure.
Wafaa El-Sadr (Harlem Hospital, New York) reported that 18 percent remain innocent of antiretrovirals, 82 percent have tried NRTIs, 69 percent PIs, and 35 percent NNRTIs.
She split the cohort into four groups classified by risk factors at the end of four years -- 2000, 2001, 2002, and 2003. She defined high risk as having an earlier MI or stroke, having diabetes, or having two or more of the above risk factors. So the precise effect of a worldwide turn to NNRTIs and to ATV in the past several years -- if any -- remains unknown in this cohort. And to this day Klein cannot make that link, though his case-control comparison now embraces 5,162 HIV-infected men tracked for 25,251 person-years and 42,531 controls followed for 295,005 person-years.
At the study's starting point, reported Rodolphe Thiébaut (University of Bordeaux, France), 127 of 233 cohort members (60 percent) took a PI regimen, 138 (59 percent) smoked, five (2 percent) took fibrates, and none statins. At this point the 36-month prevalence of lipid-clipping therapy measured 17 percent, non-PI therapy 60 percent, and smoking 51 percent. The statistical gravitas of snuffing cigarettes ebbed some with further adjustment for age, gender, body mass index, and total cholesterol (p = 0.11). And over half of the ACTG enrollees who succumbed to heart disease had less than a 10 percent baseline risk on the Framingham scale. But it's always nice to see independent confirmation of those trends in a biggish cohort -- something provided at CROI by Esteban Martínez (Hospital Clinic, Barcelona) and colleagues in the Spanish ATV early-access program [abstract 850]. At the 2005 conference a much bigger double-blind, placebo-controlled comparison of another fish oil physic, Maxepa, significantly purged high triglycerides after eight weeks, and that drop held up through week 16 [abstract 39]. For most people (63 percent assigned to TDF and 74 percent assigned to ABC), that regimen did not include a PI. One person stopped TDF because of toxicity, and three dropped ABC for that reason -- all with a hypersensitivity reaction.
Study participants taking a non-PI regimen also did somewhat better with TDF (+432 g versus +247 g). Vincent's Hospital, Sydney) noted that more people assigned to TDF took d4T at baseline (77 percent versus 59 percent assigned to ABC). Follow-up in this single-center study began before the recommendation to trim ddI doses with TDF, so the initial ddI dose was 400 mg in people weighing over 60 kg and 250 mg in those weighing less.
Not since the days of the "Berlin patient" has the HIV world put a single person under such a big microscope, as the media cheered on. At the 12th CROI, Martin Markowitz (Aaron Diamond AIDS Research Center, New York) offered a richly detailed poster printed in agate type, and those sundries appeared a few weeks later in a free-access Lancet article.16 Nor will this article broach the battle royal over the propriety of announcing the case at a press conference (except to imagine the ugly fracas if the case leaked before formal disclosure).
Whoever suggested the original acronym GRID -- for gay-related immune deficiency -- must be happy that tag didn't stick. More testing, one could speculate, may reflect more trips to the sexually transmitted disease (STD) clinic for syphilis and lymphogranuloma venereum (LGV), the frightening emerging STD considered below.
In a cluster of 12 Parisians infected with the same HCV strain, two declined anti-HCV therapy.
In the contest to give bed or needle partners drug-resistant HIV, Diane Bennett reported, neither gays nor straights, whites nor blacks, women nor men, youngsters nor oldsters have pulled into a clear lead. They now start treatment of acute infection with a boosted PI regimen until they get genotyping results.
More people in the clinic population were men (90 percent versus 68 percent) and gay (65 percent versus 39 percent), while the state program had a higher proportion of blacks (61 percent versus 43 percent). Decoding virus from 104 recently infected people with samples from two or more time points, he found viruses with highly divergent sequences in seven people.
Grant suggested that this trend "may reflect a window period for susceptibility (as in nonhuman primate research), or seroconverters may harbor several viruses that appear sequentially due to viral escape for immunologic reasons." Superinfection may become rarer during chronic HIV infection because of (1) specific antiviral immune responses to partner viruses, (2) viral interference, or (3) nonspecific immune responses. Before an HIV antibody test even signals infection, virus-induced inflammation burns though the bowels, replacing healthy mucosal tissue with collagen. And until the past year or two, the tropics were the only place one saw more than the odd case of LGV, the hard-to-diagnose, writhesome chlamydial infection that can rock the rectum and boost the risk of HIV transmission. They counted three LGV cases in 2002, 18 in 2003 (13 in the last quarter), and 102 in the first 11 months of 2004. Constipation, inguinal ulceration, and inguinal lymphadenopathy also characterize this disease.
Because the earlier Dutch LGV outbreak involved gays in Rotterdam, he wondered if the STD made an earlier debut in Amsterdam. In many HIV clinics, MRSA causes more community-acquired staph infections than methicillin-sensitive S.
Rieg and UCLA colleagues explored a nasal route, hypothesizing that gay men with HIV carry MRSA more often than MSSA in nasal secretions.

MRSA proved more common among African Americans (five of eight cases) and among people with a college education (seven of eight). One could just as readily wax wrathful over down-low black guys whose crypto-flirtations expose their girlfriends to HIV, or over straight African dandies who prey on adolescents.
Speaking at CROI about public health worries stirred by the New York City case, Jaffe defused the fluster over using case reports to scare people into better behavior. Intrapartum exposure to nevirapine and subsequent maternal responses to nevirapine-based antiretroviral therapy. Predictors of HIV drug-resistance mutations in a large antiretroviral-naive cohort initiating triple antiretroviral therapy.
A randomised open label comparative study of Combivir + efavirenz (2 class triple therapy) versus Trizivir + tenofovir (single class quadruple therapy) in initial therapy for HIV-1 infection.
In vitro activity of structurally diverse nucleoside analogs against human immunodeficiency virus type 1 with the K65R mutation in reverse transcriptase. Low genetic barrier to resistance is a possible cause of early virologic failure in once-daily regimen of abacavir, lamivudine, and tenofovir: the Tonus study. Do protease inhibitors increase the risk for coronary heart disease in patients with HIV-1 infection? A randomized, open-label clinical trial of omega-3-fatty acid (fish oil) supplementation along with diet and exercise in HIV-infected patients with hypertriglyceridemia.
That question has been debated for years by health experts and those who feel circumcision is a form of mutilation. They found the procedure reduced the rate of infection among these men by over a 76 percent. Especially in the last few years, the conference has offered a forum for research on HIV prevention and care in the epidemic's far-flung epicenters. That conjunction led to confused cries that evil Western drug lords had unleashed a baby killer in Africa. Slowly dwindling levels of this durable drug as HIV revs its replicating engine virtually guarantee that the virus will evolve the one or more mutations that can imperil responses to this drug -- or efavirenz (EFV). But in the 40 samples with no hint of K103N on routine testing, PCR descried the mutant in 16 (40 percent). But in 46 women with no hint of Y181C on standard sequencing, real-time PCR picked it up in five (11 percent).
With a population detection limit of 0.1 percent, the PCR test routinely tracked down K103N or Y181C in samples judged mutation-free by standard sequencing (Table 1).
Retrospective study showed that 20 infants had HIV four days after birth, five by three weeks, and one by six weeks. Ten of 13 children taking NVP prophylaxis had one or more NNRTI mutations soon after treatment began. So everyone should sit up straight when a particular resistance pattern foretells shorter survival, which is what happened in a study of 1,388 British Columbians who started potent therapy from August 1996 through July 2000 [abstract 712]. But this tactic was not clinically innocuous -- Kaposi's sarcoma cropped up in one person during a drug break, and toxoplasmic retinitis in another. That finding came from a randomized comparison of 87 people taking an STI and 30 continuing treatment [abstract 679].
But this case study by ViroLogic neatly makes the point proposed in Virco's mass analysis: Expect the unexpected.
They sweet-talked 109 clinicians attending regional advisory board meetings into picking new regimens based on actual genotypic (GT), phenotypic (PT), or GT-PT data -- but with no clues from case histories. Demographics like professional degree, number of patients cared for, or self-assessed resistance acumen did not affect the results in a multivariate analysis.
She scoured the 2003 Lab Corp database to track down more than 56,000 isolates in which standard population sequencing spotted either K65R or TAMs. Thirteen people started AZT, 11 started didanosine (ddI), nine kept TDF, and five kept 3TC.
And as Glaxo's Lisa Ross observed, the results for FTC need clinical verification because she inferred the phenotypic ("fold-change") cutoff for FTC from 3TC data. The cohort is heavy in smokers, with a prevalence of 47 percent, and 42 percent have lopsided lipids. An analysis that controlled for surging treatment experience over time and the ups and downs of risks and retaliatory tactics suggested that "the risk of MI has decreased over time, possibly as a result of improved targeting of intervention to those at high risk" [italics added]. But in the northern California cohort of Daniel Klein (Kaiser Permanente, Oakland), fervid adoption of ATV and swelling prescription of lipid-lowerers may be paying off [abstract 869].
Although the HIV group still has significantly higher coronary heart disease and MI rates, coronary "event" rates stratified by duration of PI therapy and by calendar period do not climb in "a clear linear fashion" over time.
Three people had to quit ATV because of jaundice and one because of spurting transaminases. The fish tabs has no known interactions with antiretrovirals, although De Truchis did not measure drug levels.
To find out, Graeme Moyle (Chelsea and Westminster Hospital, London) randomized 105 people with moderately severe lipoatrophy to replace d4T or AZT with TDF or ABC [abstract 44].
A missing-data-equal-failure analysis of the 2005 conference (DEXA) arm-plus-leg fat at week 48 figured a 393-g gain with TDF and a 316-g rally with ABC, a nonsignificant difference (p = 0.97). Adjusting the lipid analysis for that variable, he proposed, may make the significance of these differences disappear. The cohort included 100 people who took ddI at least part of the time during follow-up, 66 who took TDF, and 191 who took d4T.
During follow-up Theresa García-Benayas (Carlos III Hospital, Madrid) and coworkers cut the ddI dose to 250 mg for heavier people and to 200 mg for lightweights. Yet, although blacks in the United States and women worldwide shoulder disproportionate burdens of this plague, some of the most pungent recent trends involve the primal "risk group" -- gay men in rich countries. Nine of the remaining 10 did not respond to antiviral therapy in six months, and the tenth responded then relapsed. But men who have sex with men (MSM) made up the largest part of the cohort by exposure group (61 percent versus 25 percent heterosexual and 14 percent injecting drug users).
The survey found 24 people (3.1 percent) with virus resistant to two or more antiretroviral groups. Her study involved 112 people with acute or recent infection who came to the Aaron Diamond Center in 2003 and 2004. Three people (3.1 percent) had virus with mutations to the first three antiretroviral classes. This trend toward swelling transmission of NNRTI mutations may reflect the relatively greater fitness of this virus compared with PI or NRTI mutants -- or even wild-type virus (see note 17). Independent analysis of virus from four of these seven at additional time points confirmed that they picked up first one HIV, then another. For those without medical training, collagen is the stuff that makes up crusty cartilage and bone -- not at all what you want in your guts.
That changed last November when Dutch health authorities cited 92 cases over the preceding 17 months -- rather than the usual one or two -- most of them in gay or bisexual men.21 At CROI, epidemiologists from France detailed an explosive outbreak there [abstract 895]. Eight (57 percent) had HIV infection, nine (64 percent) had another STD in the last year, and all had anorectal signs or symptoms.
To find out, Spaargaren analyzed 82 rectal samples from 72 men who came to the health service STD clinic with proctitis in 2002 and 2003. Mathews told IAPAC Monthly that 65 percent of those with MRSA were gay men who did not inject drugs and 12 percent were gays who did shoot up.
One observed that more resistant virus probably lurks in other vaults -- like memory cells in lymphoid tissue.
In an analysis factoring in other transmission risks, those rates meant that women trying single-dose NVP a second time had a 2.3 times higher risk of giving their infant HIV. All told, new mutations sprang up in four people (5 percent) who had not taken one- or two-drug therapy in earlier days. Zolopa and collaborators powwowed on consensus picks of "acceptable" or "unacceptable" antiretroviral options. Then she subjected those samples to powerful single-genome sequencing to nose out recondite mutations. But Cozzi-Lepri adjured all to interpret those changes with caution: Because this is a cohort study -- not a trial randomizing people to d4T or AZT -- irksome "residual confounders" may sway the results.
There may be good reasons for that dwindling, as prescribers switch from PIs to NNRTIs or to the lipid-friendly PI ATV. Also, an ACTG subset of 433 people with longer follow-up had a higher heart risk at baseline.
Maxepa's thrice-daily dosing may seem rigorous to people getting used to once-a-day antiretrovirals.
Limb fat gains were equivalent in the two groups after 48 weeks, but TDF appeared to beat ABC in a metabolic marker contest. Either way, TDF may be the safer short-term switch option, given the low but real risk of hypersensitivity with ABC.
Joel Gallant (Johns Hopkins University, Baltimore) offered a step toward that goal by comparing creatinine levels and clearance in 344 people starting TDF and 314 starting another NRTI [abstract 820]. The analysis involved only non-Hispanic whites, in whom mitochondrial haplogroup H predominates. Because the six states are Colorado, Illinois, Maryland, Michigan, Virginia, and Washington, the survey missed the biggest gay urban centers. So, although transmission of multidrug-resistant virus remains rare in the United States, it is hardly a freak phenomenon. If there is any good news here, it is that no one had mutations to the fusion inhibitor ENF and that people infected with resistant virus responded to treatment as well as those with wild-type virus.
Proctoscopic exam separated them into two groups -- 42 symptomatic men with pussy anal seepage or bloody ulcerative rectal growths, and 32 without symptoms or rectal mucosal inflammation.
Spaargaren concluded that the Dutch LGV outbreak can be traced back at least as far as 2002 in Amsterdam. That's certainly true in the Harbor-UCLA Medical Center, reported Gunter Rieg [abstract 877].
Loubser agreed but maintained that his PBMC data confirm a marked overall dropoff with time. Both groups were about three quarters male and three quarters African American, and about one third got HIV from injecting drugs. Hicks told IAPAC Monthly that he could verify no risk difference by HIV transmission category. And MRSA rates are rocketing down the road at the Owen Clinic of the University of California, San Diego, according to Christopher Mathews [abstract 142]. Retrovirus dean John Coffin (US National Cancer Institute, Frederick, Maryland) said other workers have had more success than Loubser in logging persistent mutations in PBMCs.
Every N88S in the database proved susceptible to lopinavir (LPV) and amprenavir (APV), while more than 95 percent laughed off ATV and nelfinavir (NFV). The groups also balanced well in viral load and CD4 count and diabetes rates (12 percent with TDF and 8 percent in controls).
The largest proportion of those infected with resistant virus -- but not a majority -- got infected through gay sex. The drop in clearance measured 10 percent with TDF and 6 percent with non-TDF nukes (p = 0.007).

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