Worobey et al. observe that the RNA-later they used to preserve most of the year 2000 urine samples (from the Wanie-Rukula region) doesn’t normally allow immunoblot analysis, but they managed to get past that by special procedures, and repeatedly detected p24 (a core protein of immunodeficiency viruses) in two of the ten samples. Does this perhaps suggest that if ideal procedures had been used, they would have detected p24 in more than 20% of the animals? I don’t know. However, Worobey et al.’s comment about urine antibody profiles and PCR confirmation of infection in Gombe Stream, Tanzania, implies (at the least) that many of the chimps showing the p24 profile on immunoblot analysis of urine are genuinely SIV-infected.
Interestingly, neither in the main paper, nor in the supplementary information, do Worobey et al. report on the immunoblot results on the 36 urine samples collected from further south-east (Obiatuku and Parisi) in 2003.
Note that Worobey et al. detected only one PCR-positive animal out of a total of 34+97 = 131 chimp faecal samples tested in 2000 and 2003. This is a much lower rate of detection, even when (as in 2000), samples appear to have been taken from the same (presumably infected) troupe. This suggests that either their preserving methods for faeal samples, or their methods of extracting SIV from faeces collected in the field, may have been less than ideal.
It’s worth remembering that Santiago and Sharp, using PCR amplification at Gombe Stream in Tanzania, detected SIV in 13% of faecal samples obtained from three wild troupes of Pan troglodytes schweinfurthii (Pts). Because they were at Jane Goodall’s camp, rather than truly “in the bush”, it may be that their preservation methods were more effective.
One of the arguments which people like Beatrice Hahn and Bette Korber have used to try to disprove the OPV theory has been to claim that not only is Pan troglodytes schweinfurthii (Pts) the “wrong subspecies” of chimp [this argument is addressed elsewhere], but that the rate of SIV infection in wild Pts chimps is low. This claim would appear to be incorrect. In reality, it would appear that in those chimp troupes which are infected, SIV infection rates are fairly high. Although none of the Ugandan chimps sampled in the Budongo Forest was found to be SIV-infected, Santiago and Sharp’s figure of 13% SIV infection in the wild Gombe chimps should probably be used as the benchmark for Pts infection in infected troupes, at least for the time being. With regard to Worobey et al.’s results, all one can say is that their results on the year 2000 urine samples imply (but of course do not confirm) a similar infection rate in the DRC.
It needs to be pointed out that the Parisi forest, where Worobey et al. sampled the infected chimp that gave the partial SIV sequence, is about 130 kilometres south-east of Kisangani (as the crow flies), and is not known to be one of the areas where they collected chimps for Lindi camp in the 1950s. However, the Lindi chimp-catcher Gilbert Rollais was based for several months at Wanie-Rukula, 50 kms SE of Kisangani. This means that the chimps sampled during the Bill Hamilton expedition of January 2000 (which came from the forest to the immediate north and east of Wanie Rukula) are more relevant to the events at Lindi.