Yes it is true that the 1998 Wakefield study did not specifically look for the presence of measles in gut tissue of the study children. The only association alluded to in that paper was the proximity of apparent behavioural changes with the children having received the MMR (I think a median of 12 days).
However it seems that many others are also getting their references confused. In response to The Jolly Pirate's allusion to a study of measles in gut tissue carried out by Arfez (sic), Beachcomber somewhat disingenuously linked to the Afzal paper (1) looking for measles virus in blood cells, whereas she should be well aware that Afzal's group have performed at least three studies on gut tissue; two in 1998 and one in 2000. These can easily be found on PubMed. His group's work in 2006 on peripheral blood cells was published partly in response to the Kawashima (2) findings in 2000, which claimed to have found measles virus in peripheral blood cells in autistic children (more specifically: one of eight patients with Crohn disease (aged 18?34 years), one of three patients with ulcerative colitis (aged 15?31 years), and three of nine children with autism (aged 3-10). Interestingly, Beachcomber quotes the Kawashima paper as one of Wakefield's further studies a couple of posts further on, so any criticism of the Afzal paper such as: "... if they had examined children with the correct profile it was extremely unlikely that they were going to find measles RNA in the blood of these children years after their exposure" should also apply to the Kawashima study seeing as 40% of their positives in blood were in UC and Chrohn's patients. Unfortunately, the autistic enterocolitis diagnosis is still one of Wakefield's own hypotheses (and therefore not accepted as a clinical diagnosis as such), so what can other laboratories do if Wakefield won't share his 'ethically-sourced' research specimens? Perhaps he learned his lesson from the Chadwick study (3), in which his own Inflammatory Bowel Disease Group labs found no evidence of measles RNA in IBD cases using very sensitive amplification techniques (4), and thus did not support Wakefield's earlier hypothesis about measles and IBD from 1992.
The Uhlmann paper (5) from O'Leary's lab purporting to show over 80% of samples positive for measles virus has received a number of strong criticisms, particularly because instead of using established measles primer sequences for PCR, they designed new primers for their investigation (this is also true of the Kawashima study). From the data presented in the paper, they failed to do essential preliminary work to show that their new primers were genuinely detecting measles sequences rather than amplifying non-specific regions. Not a single one of the Uhlmann measles positives was sequenced to show it was measles-specific, and later work by d'Souza (6) showed that both Uhlmann and Kawashima primers amplified non-specifically in terms of amplicon length. When blood cells from ASD cases and controls were examined using the primers, 100% of cases and 100% of controls were positive for measles with Uhlmann primers and 0% cases and 0% controls with the Kawashima primers. When sequenced, all the positive Uhlmann amplicons consisted of non-measles sequences. These results collectively make the Uhlmann/O'Leary and Kawashima findings non-repeatable under better controlled conditions, so unless someone comes up with a more impressive study, the null hypothesis has to prevail; which is that there is no association with measles and autistic enterocolitis from the published laboratory studies.
(1) Afzal MA, Ozoemena LC, O?Hare A, et al. Absence of detectable measles virus genome sequence in blood of autistic children who have had their MMR vaccination during the routine childhood immunization schedule of UK. J Med Virol. 2006;78: 623?630
www.ncbi.nlm.nih.gov/pubmed/16555271
(2) Detection and sequencing of measles virus from peripheral mononuclear cells from patients with inflammatory bowel disease and autism.
Kawashima H, Mori T, Kashiwagi Y, Takekuma K, Hoshika A, Wakefield A.
www.ncbi.nlm.nih.gov/pubmed/10759242
(3) Chadwick N, Bruce IJ, Schepelmann S, Pounder RE, Wakefield AJ(1998). Measles virus RNA is not detected in inflammatory bowel disease using hybrid capture and reverse transcription followed by the polymerase chain reaction. J Med Virol. 1998 Aug;55(4):305-11.
www.ncbi.nlm.nih.gov/pubmed/9661840
(4) Chadwick N, Bruce I, Davies M, van Gemen B, Schukkink R, Khan K, Pounder R, Wakefield A.
A sensitive and robust method for measles RNA detection.
www.ncbi.nlm.nih.gov/pubmed/9506813
(5) Potential viral pathogenic mechanism for new variant inflammatory bowel disease. Uhlmann V, Martin CM, Sheils O, Pilkington L, Silva I, Killalea A, Murch SB, Walker-Smith J, Thomson M, Wakefield AJ, O'Leary JJ.
www.ncbi.nlm.nih.gov/pubmed/11950955 (full paper free to read)
(6) No evidence of persisting measles virus in peripheral blood mononuclear cells from children with autism spectrum disorder. D'Souza Y, Fombonne E, Ward BJ.
www.ncbi.nlm.nih.gov/pubmed/17015560 (full paper free to read)