New light on the “New York patient”: `super-bug` fears were exaggerated by media

Derek Thaczuk
Published: 10 April 2007

In early 2005, a gay New York City man was reported to have been infected with an extremely virulent, multi-drug-class-resistant (MDR) strain of HIV, causing very rapid progression to extremely low CD4 cell counts. Public health officials in the city raised the alarm, and US newspapers reported that a new, highly aggressive drug-resistant strain of HIV was at large in the city's gay male population.

But now, two years later, the first comprehensive report on the case in a medical journal shows that almost all the initial media - and public health - assumptions about the case turned out to be wrong.

Ongoing analysis of the “New York City patient” has now suggested that he may have been initially infected by a dual-(CXCR4 and CCR5) –tropic virus, rather than having developed it himself, and that the case was highly unusual. The analysis also suggests that his rapid CD4 count drops were associated with primary infection, rather than the extremely rapid chronic infection first reported. The new analysis and commentary are published in the May 1st Journal of Infectious Diseases.

The original case was extremely well publicised; the most pertinent facts about the NYC patient were as follows:

  • Diagnosed HIV-positive in December 2004.
  • The date of his infection was not certain, but was no more than 20 months prior to diagnosis.
  • He was a heavy crystal methamphetamine user who had frequent, anonymous, unprotected sex.
  • He was deemed a rapid progressor and diagnosed with AIDS based on low CD4 cell counts (80 cells/mm3 at diagnosis, 28 cells/mm3 in January).
  • His virus was dual (CXCR4 and CCR5) -tropic, multi-drug resistant (although susceptible to efavirenz and T-20), and actually had higher replicative fitness than wild-type (1.38-fold fitter) despite its resistance mutations.

The source of the NYC patient’s infection (the “source patient”) was soon identified. His viral strain was also found to be highly drug resistant, but much less fit (.041-fold compared to wild-type), and apparently CCR5-tropic only. The source patient was not a rapid progressor; he had been on various antiretroviral combinations since 1995.

The source patient’s regular sexual partner was also identified, and found to have been superinfected: he was carrying a recombinant MDR strain of his own original virus (which had been drug-susceptible up until 2001), and the source patient’s.

Two years later: Why did the NYC patient progress so quickly?

The newly published report by Gary Blick (the source patient’s physician, who reported on the case at the 2005 IAS conference) and team provides further detail, and advances some possible answers to unanswered questions from 2005.

It now appears virtually certain (from subject interviews) that the NYC patient was infected on October 22, 2004. The NYC patient’s initial AIDS diagnosis and status as a “rapid progressor” were solely based on CD4 counts: he showed no major clinical signs of disease progression other than fever, sore throat, weakness and fatigue, and a 4kg weight loss.

Questions arose at the time as to whether primary infection could have explained the rapid CD4 count drop, as counts often drop dramatically in the first three months after infection, recovering as the infection enters its chronic phase.

The NYC patient was assessed at the time to be beyond the acute infection phase: however, it now appears that he had been infected for less than two months at the time of diagnosis.

This could imply that the very low CD4 counts seen in early 2005 were in fact transient and due to primary infection, rather than progressive and due to chronic disease. (This is not confirmed by the Blick report, which focuses on the source patient and his partner, and does not describe the NYC patient’s medical history since the 2005 reports.)

Extensive analysis of the source patient’s viral phenotype confirms that, although he shared an extremely similar viral strain with the NYC patient, he did not show signs of rapid progression. “This suggests that host factors as well as, or instead of, the virus were important in the pace of [the NYC patient’s] disease progression,” states the editorial commentary by Frederick Hecht and colleagues.

How did the virus become dual-tropic?

Samples collected in October 2004 show that the source patient’s virus was predominantly CCR5-tropic, leading to concern that dual-tropic virus had evolved extremely quickly in the NYC patient (a process that normally occurs over years of chronic infection).

However, samples collected from the source patient a year later, in October and November 2005, do show mixed-tropic virus. The report suggests that dual-tropic virus may in fact have been present in the source patient’s seminal fluid, but not detected in blood plasma, at the time he infected the NYC patient. This would negate the prior concern that we were seeing a viral strain capable of extremely fast evolution to a dual-tropic form.

The source patient was also reportedly non-adherent to his antiretroviral treatment, which could potentially have driven the switch in tropism.

Superinfection and implications for serosorting

In 2005, only 23 cases of superinfection had been described. Evidence indicated that superinfection was more common in more recently infected individuals (<3 yrs) but rare in the chronically infected – presumably due to a “build-up of innate immune responses.”

However (as reported previously) the source patient’s partner, despite having been diagnosed HIV-positive in 1994, became demonstrably superinfected as well. The researchers now describe this as “the first case whereby a chronically HIV-1-infected, heavily ARV therapy-experienced individual… may have become superinfected by a second distinctly different subtype… after years of serosorting with other chronically HIV-1-infected partners”.

The commentators “believe that existing evidence continues to suggest that superinfection… is uncommon after the first few years of infection, and this report should not lead to the abandonment of serosorting as one strategy to reduce HIV transmission. However, this case is an important cautionary tale that drug-resistant HIV truly can be transmitted to a chronically HIV-infected partner.”


Blick G et al. The probable source of both the primary multidrug-resistant (MDR) HIV-1 strain found in a patient with rapid progression to AIDS and a second recombinant MDR strain found in a chronically HIV-1–infected patient. J Infect Dis 195:1250-1259, 2007.

Hecht FM, Wolf LE, Lo B. Lessons from an HIV transmission pair. J Infect Dis 195:1239-1241, 2007.

Blick G et al. “Patient Zero”: the Connecticut source of the multi-drug-resistant, dual-tropic, rapidly progressing HIV-1 strain found in NYC.Third International AIDS Society Conference on HIV Pathogenesis and Treatment, Rio de Janeiro, Abstract MoOa0101, 2005.

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