Levamisole adulteration rates have been increasing nationally over recent years. Using a national forensic laboratory database, the U.S. Enforcement Agency (DEA) Office of Diversion Control recently reported a five-fold increase in levamisole-tainted cocaine since 2007.

“Substances identified by federal, state and local forensic laboratories, as containing levamisole, increased from 712 in 2007 to 3,630 in 2010,” states a DEA drug intelligence brief.

The DEA has internally tracked and reported in Microgram, the agency’s in-house forensic sciences publication, the suspicious rise of the adulterated cocaine since 2003, when less than 5 percent of cocaine seized in the U.S. contained levamisole.

A growing body of scientific literature and case reports from the medical community reveal the dermatologic, cardiac, immunologic, and vascular manifestations of levamisole-laden cocaine. The study titles and associated images are grim – ranging from necrotic vascular lesions to raging skin and soft tissue infections in the setting of levamisole-depleted white blood cells counts.

Now there is even concern over additional cardiopulmonary risks over and beyond those reported from non-adulterated cocaine, according to a 2011 International Journal or Cardiology report.

National attention focused on the issue in September 2009 when the Substance Abuse and Mental Health Services Administration (SAMHSA) issued a Nationwide Public Health Alert warning of the life-threatening risks associated with levamisole.

First introduced as a de-worming agent in the 1960’s and believed at the time to be safe in single doses, levamisole had a second debut in the early 1990’s as an FDA-approved chemotherapy for colorectal cancer, only to be voluntarily removed from the market in light of a spectrum of adverse events — most notably depleted white blood cell counts known as agranulocytosis.

Now, levamisole has a strange new career as it is introduced in cocaine manufacturing countries. Levamisole’s novel optical properties approximate those of cocaine and the adulterant is relatively cheap and easy to acquire, according to sources interviewed by Brandon Kiley, a Seattle-based journalist who wrote the seminal series, “The Mystery of the Tainted Cocaine.”

As national awareness of the adulterant has, the number of case reports in the medical literature has predictably sky-rocketed. In the first six months of 2011, the total number of publications concerning levamisole and cocaine has doubled.

Many of the new reports simply repeat Department of Justice statistics about prevalence, but a 2011 report by an enterprising group in the Journal of American Medical Assocation crafted their own prevalence study independent of seizure statistics. They sampled hundreds of cocaine positive urine samples over a three months period and learned that 78 percent of the cocaine positive samples contained levamisole.

Is levamisole converted to a stimulant in humans?
Many recent case reports underscore levamisole’s known vascular and immunologic risks, but novel findings in the sea of levamisole and cocaine are also at hand.

The International Journal of Cardiology recently published a study by Berkeley, Calif.-based toxicology and pathology consultant Steven B. Karch and others, underscoring the intriguing possibility that levamisole potentiates the euphoric effects of cocaine by way of conversion into a novel psycho-stimulant.

While the scientific reporting is sparse, the cardiology study provides evidence from cocaine-positive urine samples that levamisole is coverted in humans to the stimulant aminorex.

A 2009 scientfic paper demonstrated this conversion in race horses, but the data on humans to date has been limited.

Aminorex has had a disastrous medical history, including a five-year epidemic between 1967 and 1972 of idiopathic pulmonary hypertension (IPH) in Switzerland, Austria, and Germany, “where the drug was promoted and approved for weight loss purposes, the team reports,” Karch and his coauthors wrote.

A relationship between anorectics, cocaine abuse, and IPH was first proposed more than 40 years ago.

“Even those who did write about a possible relationship between cocaine and IPH had no idea how, or even if, the cocaine abused by the patients had been adulterated,” they wrote.

Are some individuals more susceptible than others?
Another recent study suggests genetic susceptibility to the immunologic influences of levamisole.

The study, published in the American Journal of Clinical Pathology last year, revealed an association for increased immunologic susceptibility among certain individuals with a predisposing human leukocyte antigen (HLA). The HLA system helps the body screen the identity of cells as either foreign or self-made and confusion in this system can lead to states where the body attacks itself.

“In our series, three (60percent) of five patients with cocaine-associated agranulocytosis for whom testing could be performed were HLA-B27positive; in contrast, the local population frequency of HLA-B27 is 8.5 percent,” reported DR Czuchlewski and co-authors – suggesting greater susceptibility to adverse events among cocaine users with predisposing HLA status.

HLA-B27+ carriers are also known to be more susceptible to spondylitis, an inflammatory disorder of the spine and pelvis.

Harm-reduction strategies, policies little studied

Little attention has been paid to harm-reduction strategies and other policy initiatives might be employed to raise public awareness of the danger or reduce the health effects of levamisole.

Diane Rimple, an Emergency Department physician in New Mexico and a co-author of the 2009 CDC report documenting adverse levamisole reactions in four states, wonders if there will be joint government/pharmaceutical industry effort to introduce a standard dye into batches of levamisole worldwide, to deter diversion into cocaine manufacturing.

The cost and feasibility of such a policy is not yet clear.

“This presents an opportunity for the DEA and pharmaceutical industry to develop a cooperative initiative to create deterrents to levamisole diversion,” Rimple says. “Simple changes in properties of levamisole could make it detectable without sophisticated equipment – by alerting its color, texture, size or smell.”

Others have proposed harm reduction strategies that are in the works.

University of Washington Assistant Professor of Psychiatry and Behavioral Science Michael Clark has invented a field-testing kit for levamisole, which is being distributed free of charge to drug users in Washington state. While the kit’s outcomes and effects on cocaine use remain unknown, it is the only active harm reductions measure currently available in this setting.

But why that relationship exists is unclear.

“Attained adult height is unlikely to directly modify cancer risk,” notes University of Manchester oncologist Andrew G. Renehan in an accompanying commentary.

But evidence that childhood nutrition or illness are to blame, is “mixed and indirect,” Renehan cautions.

One potential factor is insulin-like growth factor (IGF)-1, circulating blood concentrations of which strongly predict childhood growth and some adult cancer risks, Renehan notes.

Authors of the new study used data from the UK National Health Service’s Million Women Study of more than a million middle-aged volunteers recruited between 1996 and 2001. Study participants were diagnosed with 97,376 cases of cancer.

Researchers found that height increased women’s risk for 10 of the 17 cancer types studied: colorectal cancers, malignant melanoma, breast, endometrium, ovary, kidney, brain, non-Hodgkin lymphoma, and leukemia.

Overall, every additional 10 cm (3.9 inches) in a woman’s height was associated with a 16 percent rise in her total cancer risk.

A meta-analysis pooling data from the study and ten other studies, found the relationship between height and cancer holds true around the world, with little variation across populations in Europe, the Americas, Asia and Australia.

While previous smaller studies found a relationship between height and cancer risk for individual cancer types in both men and women, the new study of women included potentially-confounding lifestyle measures like alcohol and tobacco use, exercise and reproductive history. The relationship between height and cancer was not affected by socioeconomic status, exercise habits, alcohol drinking habits or other factors studied, they found — except tobacco smoking status. (The relationship between smoking-related cancers and height was weaker among smokers.)

Body Mass Index (BMI) — calculated using both patient weight and height — also predicts cancer risk.

But that relationship may in some cases be confounded by height, Renehan speculates.

BMI is inversely associated with premenopausal breast cancer risk, for example — but that relationship may be driven by height, he notes.

“In the future, researchers need to explore the predictive capacities of direct measures of nutrition, psychosocial stress and illness during childhood, rather than final adult height,” Renehan writes.

Further reading:

Green J, et al. Height and cancer incidence in the Million Women Study: prospective cohort, and meta-analysis of prospective studies of height and total cancer risk. The Lancet Oncology, Aug. 2011;12(8):785-794. doi:10.1016/S1470-2045(11)70193-0.

Renehana AG. Height and cancer: consistent links, but mechanisms unclear. The Lancet Oncology, Aug. 2011(8);12:716-718.

One politically-sensitive Army report excluded from the disclosed list is a 2005 EPICON study detailing the spread of multidrug-resistant Acinetobacter infections from contaminated military hospitals in Iraq throughout the military hospital system.

That report details evidence that that improper use of antibiotics and unsanitary conditions at U.S. military hospitals were responsible for the deadly outbreak of Acinetobacter infections among wounded troops, and that the outbreak had spread to civilian patients in the U.S. and Germany, killing several of them.

But for several years after the study’s completion, Army health officials continued to downplay the risk to civilians and to make misleading statements to soldiers and the public, claiming Acinetobacter infections were from Iraqi soil in soldiers’ blast wounds.

In reality, Acinetobacter “wound infections were relatively uncommon,” the 2005 Acinetobacter EPICON report states. “Pre-hospital, primary wound infections in-theater are not likely to have a significant role in transmission.”

In Iraq, military surgeons were using broad-spectrum antibiotics as prophylactics against infection, “introducing a greater risk of multi-drug resistant organisms (MDRO) evolving as a result,” the report notes.

Hand hygiene practices were inconsistently observed by military healthcare workers, the report states.

“Proper hand washing has been the single most important measure in controlling hospital spread of Acinetobacter,” the report states.

All seven military hospitals in Iraq were found to be “contaminated” with Acinetobacter, the report states.

Civilians were at much greater risk from infections than soldiers, the report states.

The report recommended adoption of standardized infection control practices at military hospitals and the air evacuation system, including disinfection and hand washing practices – and noted a pressing need for improved medical record-keeping “at all levels of care, particularly in-theater.”

A German hospital accepting U.S. troops on a referral basis, experienced an Acinetobacter outbreak that spread to German patients, the report states. That outbreak “reflects the potential importance that the outbreak can have, and probably has had, outside of the direct chain of evacuation,” the report states. Similar outbreaks had occurred in British hospitals where UK troops had been treated, the report notes.

Missing and incomplete medical records complicated the study, the report states.

“Relatively few surveillance and infection control data are available from in-theater, although progress has been made,” the report states. “Data quality from patient chart reviews indicates large variation in data available and no standardization.”

The “absence of good documentation either precludes any ability to draw scientific conclusions or significantly complicates investigations and analyses that are critical for prioritizing interventional resources and saving lives,” the report states.

epiNewswire’s Bryant Furlow first reported on an Acinetobacter outbreak among Iraqi and U.S. patients on the U.S. Navy’s hospital ship Comfort in July 2006, in the International Affairs Journal’s International Update newsletter.

In February 2007, Wired magazine writer Steve Silberman subsequently broke the story of Acinetobacter’s spread to Europe, Walter Reed Army Medical Center, and elsewhere. Silberman’s report details how the family of a U.S. Marine who died of his infection, was initially told he had died of his wounds.

That summer, citing two medical journal publications based on parts of the EPICON research effort,  Reuters reported that “new research” showed that contaminated hospitals, not Iraqi soil, caused the Acinetobacter outbreak.

In reality, military medical officials had suspected as much since spring 2003, the EPICON report indicates — and had known it to be the case since the first, 2004 symposium on the project’s initial findings.

Further reading:

EPICON #12-HA-01-JK-04, “Investigating Acinetobacter baumannii infections at U.S. Army military treatment facilities 27 August 2004 to 27 May 2005.” (View here, via Document Cloud.)

Steve Silberman. “The invisible enemy.” Wired magazine, February 2007.

Reuters Health. “Field hospitals source of soldier infections.” June 18, 2007.

No mention is made in that list of any 2010 or 2011 EPICON studies. Nor is there mention in the list of a 2005 EPICON report on the origins and spread of multidrug-resistant Acinetobacter bacterial infections throughout the military hospital system, and from veterans to civilians in Germany and the U.S. (See related story.)

The list of disclosed studies can be found below.

In a cover letter accompanying the incomplete list of EPICON study titles, Army Public Health Command Deputy Chief of Staff for Communication/FOIA Kevin M. Delaney offers no mention of, or explanation for, the omission of some EPICON report titles from the disclosed list.

Explanations for withheld material are required under FOIA.

Delaney indicates in the letter that digital copies of EPICON reports completed in 2010 and 2011, requested in February, would be provided no later than May 30, 2011. The delay in disclosing the 2010 and 2011-completed EPICON reports was “due to the volume and the complexity of the information that must be reviewed,” Delaney wrote.

But no such study titles are noted in the two-page list of completed EPICON reports accompanying his letter.

In an attempt to confirm an unsubstantiated report that some politically-sensitive EPICON projects had been suspended before completion, epiNewswire had also requested the titles and start dates for all incomplete EPICON studies.

But Delaney declined to provide such lists, writing that they could not be released “because ongoing reports would not be considered a federal record.”

epiNewswire has reported previously on the censorship of politically-sensitive medical research by military researchers under the so-called Actionable Medical Intelligence (AMI) censorship program.

The two-page list of EPICON studies lists the following completed research projects. (The 2005 EPICON #12-HA-01-JK-04, “Investigating Acinetobacter baumannii infections at U.S. Army military treatment facilities 27 August 2004 to 27 May 2005,” was not included in this list.)

12-MA-5762-0: Victory Fitness Program: Influence of the US Army’s emerging physical readiness training doctrine on fitness and injuriesin basic combat training, 2000.

29-HE-2682a-00: A second investigation of injuries among officers attending the US Army War College, Carlisle Barracks PA, during Academic Year 2000.

29-HE-1395-00: Determining physical fitness criteria for entry into US Army Basic Combat Training, 2000.

29-HE-5711-00: Investigation of an acute respiratory disease outbreak due to Adenovirus Type 4 among recruits, Fort Benning, Georgia, April-May 2000.

12-MA-6558-01: Evaluation of injury rates during implementation of the Fort Drum Running Show Injury Prevention Program, 2001.

11-HC-01L1-03: Severe pneumonia during Operation Iraqi Freedom, March-August 2003.

13-HG-04HT-06: Investigation of possible transmission of tuberculosis infection among combined Joint Task Force-76 personnel, Bagram Air Field and Kandahar Air Field, Afghanistan 3 Oct – 3 Nov 2005.

13-HG-00L8-06: Multiple serogroup meningococcal cluster among a Department of Defense population in Germany, Jan – Mar 2006.

13-HG-06TU-07: Investigation of two intestinal botulism cases at Fort Meade, Maryland, October – December 2006.

23-MA-083E-08: Risk factors for injury and cigarette smoking and temporal trends in demographic and lifestyle characteristics among US Army Ordnance School students 2000-2006.

12-MA-08LR-08: Investigation of completed suicides at Fort Campbell, Kentucky, November – December 2007.

11-HC-05UB-09: Investigation of Human Immunodeficiency Virus infection among veterans of Operation Enduring Freedom and Operation Iraqi Freedom, and execution of the Army HIV Program, October 2001 through September 2007.

14-HK-OB1U-09: Investigation of homicides at Fort Carson, Colorado November 2008 – May 2009.

“We consulted with the Department of Justice and concluded this request is too broad in subject matter,” FOIA officer Kevin M. Delaney wrote in a FOIA denial letter postdated May 5, 2011. “Therefore, we have denied this request.”

epiNewswire had requested the documents in a Freedom of Information Act (FOIA) request dated Feb. 15, 2011.

The FOIA request sought a list of the titles and dates of Army epidemiolgoical consultation (EPICON) reports conducted since 2001 and completed EPICON reports dated 2010.

epiNewswire also sought the titles and start dates of all incomplete EPICON studies.

EPICON studies are undertaken by teams of epidemiologists and other scientists, like microbiologists, when unexplained health problems or disease outbreaks occur in military populations. Typically, only two or three such studies are undertaken in a given year. epiNewswire is preparing an appeal of the denial decision and has filed new FOIA requests with the Army Public Health Command, for the alleged Department of Justice opinion and other correspondence.

2010 saw 7,270 deployed troops hospitalized or treated for TBIs, or about 20 new cases per day, the report shows.

That is more than any other year between 2003 and 2010, and represents a 34 percent jump from 2009′s count of 5,818 soldiers with TBI. Only 2008 came close to matching the 2010 numbers, with 7,263 soldiers with brain injuries during deployment. Between 2003 and 2010, a total of 33,446 soldiers have been hospitalized or treated for TBIs during or within 30 days of deployments, according to the report.

Only raw counts, not incidence rates, were described in the report.

The actual numbers are likely higher than reported, however. Data for 2010 was compiled in January and February 2011, for example, before administrative records for hospitalizations in late 2010 had all been reported. And even though the Pentagon acknowledges TBI symptoms may not emerge, or may not be recognized, until after soldiers return home from combat deployments, the new study only reports TBIs diagnosed during deployment or within 30 days of the end of a soldier’s deployment. Furthermore, a footnote in the report reveals that more than 2,700 soldiers hospitalized or treated for TBI during deployment were excluded from analysis because of pre-deployment histories of TBI. 

Only a soldier’s first TBI diagnosis is counted, so the report does not reveal how many soldiers have suffered repeated brain injuries. 

Reported brain injuries prior to 2008 are also likely underestimates.  During that time, military physicians noted in memos obtained by epiNewswire that reporting of combat injuries was incomplete. And as epiNewswire revealed in 2007, the Army had not yet implemented by that year a long-standing order to screen returning combat veterans for brain injuries.

Last year also saw a dramatic rise in amputations during or within a year of deployment, from 88 amputations in 2009 to 182 in 2010, the report shows. That’s more than any year of combat operations in Iraq and Afghanistan except 2007, when 205 soldiers underwent deployment-related amputations.

A total of 1,138 soldiers had deployment-associated limb amputations between 2003 and 2010, according to the new report.

The report shows a slight increase in sand fly-vectored leishmaniasis infections (called the “Baghdad boil” by soldiers), from 48 cases in 2009 to 65 cases in 2010. While those numbers likely represent genuine declines from the 622 cases reported in 2003, epiNewswire reported in 2007 that the Army had curtailed field reporting of leishmaniasis infections from Iraq, resulting in underestimations of actual infection rates.

The new report was released March 4, and details the numbers of deployment-associated TBIs, pulmonary emboli and deep-vein thrombosis, amputations, heterotopic ossification (aberrant bone growth following trauma), severe pneumonia, and leishmaniasis between 2003 and 2010.

Source: U.S. Armed Forces Health Surveillance Center. Deployment related conditions of special surveillance interest, U.S. Armed Forces, by month and service, January 2003-January 2011 (data as of 01 March 2011). Medical Surveillance Monthly Report, February 2011;18(2):13. (Report released March 4, 2011.)

It has been known since the early 1980s that the risk of developing acute myeloid leukemia (AML, a red blood cell cancer) is associated with benzene exposure, thanks largely to pioneering work by U.S. Occupational Safety & Health Administration (OSHA) epidemiologist Peter Infante. Based primarily on AML findings, the International Agency for Research on Cancer (IARC) has classified benzene as a group 1 human carcinogen.

But benzene’s associations with other blood and immune cell cancers, like lymphoblastic (white blood cell) leukemias, multiple myeloma, and lymphomas, have been more controversial. Studies showing associations have been contested by industry researchers, who pointed to other studies failing to show any such links.

But the new meta-analysis supports an association between occupational benzene exposure and the risk of at least three of these cancers: myeloma, acute lymphoblastic leukemia (ALL) and chronic lymphoblastic leukemia (CLL), report authors at Utrecht University in the Netherlands and the U.S. National Cancer Institute in Bethesda, MD.

The analysis also reveal that higher-quality studies yield higher risk estimates for myeloma and lymphoblastic leukemias than do low-quality studies, they report. Among other problems, low-quality studies had smaller sample sizes and poor documentation of benzene exposures, they report.

“Inadequate documentation, uncertain quality of follow-up and, most problematic, potential inclusion of ‘unexposed’ workers in ‘exposed’ categories would likely have resulted in attenuation of the observed associations,” they write. “(S)tudies that reported higher (and more significant) risk ratios for AML generally also reported higher risk ratios for NHL (non-Hodgkin lymphoma), myeloma, ALL and CLL.”

They found no association between benzene and Hodgkin’s lymphoma.

The association with NHL was “less clear,” the authors report. Although NHL risk estimates increased with increasing study quality, associations between NHL and benzene failed to reach statistical significance, the authors note. But this could be because NHL is a collection of diverse cancers, some of which may not be associated with benzene exposure, they suggest.

“The evidence for an association between benzene and NHL is less convincing, but this could be explained by the heterogeneity in the association for particular subgroups of this disease or by not accounting for certain biases,” the authors report.

As reported by epiNewswire in 2010, the journal in which the study was published, Environmental Health Perspectives, recently removed mention of benzene from a review of the causes of childhood ALL, despite evidence — confirmed in the new meta-analysis — that adult ALL is associated with benzene exposure.

Further reading:

Vlaanderen J, Lan Q, Kromhout H, et al. Occupational benzene exposure and the risk of lymphoma subtypes: a meta-analysis of cohort studies incorporating three study quality dimensions. Environmental Health Perspectives. 2011. 119:159-167. DOI:10.1289/ehp/1002318

Among Acinetobacter’s “copious genetic resistance mechanisms” are an arsenal of enzymes that can alter antibiotic drug molecules, rendering them ineffective, and bacterial cell wall adaptations that deny antibiotic drugs attachment or entry sites, report researchers researchers from Chicago-area hospitals and universities.

For example, resistance to beta-lactam antimicrobials involves a frontal assault on drug molecules, the authors report; the bacteria excrete beta-lactam-specific enzymes that degrade the drug.

These genetic adaptations spread rapidly because they are readily shared with other baceteria through plasmid exchange within complex multi-species biofilms that can form on patients’ tissues or hospital surfaces, research has shown.

Resistance to tetracyclines, fluoroquinolone and aminoglycoside medications, on the other hand, involves efflux pump mutations. Polymyxin resistance appears to be related to genetic mutations that ruduce the number of bacterial wall pores.

Infectious disease epidemiologists have been issuing increasingly urgent calls for the development of new classes of antibiotics to circumvent Acinetobacter’s defenses.  epiNewswire carries continuing coverage of Acinetobacter research news.

Further reading:

Esterly J, et al. Genetic mechanisms of antimicrobial resistance of Acinetobacter baumannii. Annals of Pharmacotherapy. 2011 (Feb). DOI 10.1345/aph.1P084

But that figure is based on the implausible assumption that current cancer rates, cancer survival rates, and medical costs don’t change.

If the costs of new diagnostic tools and treatments continue to rise, costs will be much, much higher, the authors caution — a projected $207 billion a year. Improving survival rates will also likely drive overall costs up, they note. The study was based on Medicare expenditures and data from the NCI’s national cancer surveillance program, called SEER.

“If we assume a 2% annual increase in the average costs of care in the initial and last year of life phases, the cost of cancer care is estimated to be $172.77 billion, representing a 39 percent increase” over 2010 costs, lead author Angela Mariotto writes. “Costs of cancer care in 2020 were estimated to be $207 billion under the assumption of 5-percent increase in the costs in the initial and last year phases of care (escalating costs), representing a 66 percent increase from 2010.”

Caring for breast cancer patients alone will cost $20.5 billion a year by 2020, Mariotto’s team projects.

The authors did not comment on the implications of these rising costs for Medicare cost control efforts, evidence-based oncology or implementation of the federal health reform law.

Further reading:

Mariotto AB, et al. Projections of the cost of cancer care in the United States: 2010-2020. Journal of the National Cancer Institute. 2011;103(2):117-128. doi:10.1093/jnci/djq495.

A genetic “match” between the viral strain infecting rapist and victim is frequently presented to juries and TV audiences with certitude, as a molecular smoking gun. That seemingly compelling piece of evidence is “increasingly determining convictions by criminal courts,” according to six European virologists in the current issue of The Lancet Infectious Diseases.

But calling the comparison of HIV strains’ genes “fingerprinting” — calling to mind the more-familiar matching of human suspects’ DNA to blood at a crime scene — is dangerously misleading, they warn.

“By calling such investigations HIV fingerprinting, scientists raise unrealistic expectations” about the method’s accuracy among juries and judges, the write. “Unlike for (human) DNA fingerprinting, where a likelihood can be calculated for a full match between the evidential DNA and the suspect’s DNA, there is never a full match between the RNA or the DNA of HIV in two samples, even within an individual.”

That is partly because HIV strains are constantly evolving, they note.

“Proper identification of the transmission source would require two major assumptions: that a phylogenetic tree can flawlessly reconstruct a true epidemic history and that strains from all patients ever infected with HIV are available as controls,” the authors write. “Both assumptions are unrealistic.”

Worse, since the full range of local genetic variation and the relatedness of local HIV strains are unknown, the probability that one individual’s HIV infection came from another specific individual simply cannot be quantified, the authors note.

“Because the full transmission tree is unknown, no likelihood can be attached to the a priori hypothesis of direct transmission,” they write.

Indirect routes of infection through third parties can never be ruled out, and the rapid evolution of strains could inaccurately clear a real rapist, they caution.

“Phylogenetic analysis is a powerful technique that can, if properly used, provide valuable circumstantial evidence in forensic investigation for cases of HIV transmission,” they conclude. “However, scientists should be aware of the limitations of this analysis, and should emphasize that courts must use other evidence to achieve a conviction.”

The authors recommend six best practices to avoid misuse of viral phylogenetic data in criminal cases, including the use of two samples from different points in time from each party under investigation as close in time to the alleged transmission, to analyze more than one region of the viral genomes, and for testifying scientists to make no claims or estimates of the statistical probability of direct transmission.

The authors declared that they have no conflicts of interest.

Further reading:

Abecasis AB, et al. Science in court: the myth of HIV fingerprinting. Lancet Infectious Diseases. 2011(Feb);11:78-79.

Gilbert N. Science in court: DNA’s identity crisis. Nature. 2010;464:347-348.

Shankarappa R, et al. Consistent viral evolutionary changes associated with the progression of human immunodeficiency virus type 1 infection. Journal of Virology. 1999;73:10489-104502.