T 0111/10 (Diagnosis of spongiform encephalopathy/D-GEN) 24-06-2014

Reasons for the Decision

1. The appeal is admissible.

2. Main request: Article 123(2) EPC

2.1 The present opposition did not cite Article 100(c) EPC as a ground of opposition. However, as confirmed by the Enlarged Board of Appeal in its decision G 9/91 (OJ 1993, 408, reasons 19), in case of amendments of the claims or other parts of a patent in the course of opposition or appeal proceedings, such amendments are to be fully examined as to their compatibility with the requirements of the EPC.

2.2 The main request corresponds to the claims as maintained by the opposition division, and differs from the claims as granted in that "a prion or spongiform encephalopathy disease" has been replaced by "bovine spongiform encephalopathy or Creutzfeldt-Jakob disease" in claim 1. As basis for the amendments in relation to the granted claims, the respondent indicated a number of passages in the description, inter alia Figures 4, 5a, 5b and 8a, as well as page 10, lines 5 to 26; page 11, lines 12 to 15; page 12, section "Discussion"; page 26, lines 23 to 26.

2.3 The board comes to the conclusion that there is no basis in the application as filed for the combination of features "typing a sample of bovine spongiform encephalopathy" and "comparing and identifying similar (...) sizes (...) of distinct PrP**(sc) glycoforms". Of the above-mentioned passages, the only passage wherein glycoform size is mentioned in the context of bovine spongiform encephalopathy (BSE) is the passage on page 11, lines 12 to 15. This passage however is in the very specific context of transmission of BSE to wild-type mice, wherein the band sizes of PrP were shifted to a lower molecular mass as compared to type 2 Creutzfeld-Jakob disease (CJD) transmissions. There is no disclosure in the application as filed allowing to generalise this disclosure to the claimed subject-matter. In addition, although the application discloses typing of a prion disease in the sense of identifying whether said prion disease is CJD 1, 2, etc. or BSE, it does not disclose typing of a BSE disease, which would imply identifying different types of BSE disease.

2.4 Accordingly, claim 1 of the main request does not comply with the requirements of Article 123(2) EPC.

3. First auxiliary request: Admissibility

3.1 This request was only submitted during oral proceedings before the board. Hence its admission is at the board's discretion (Article 114(2) EPC), governed by the principles laid down in Article 13 RPBA.

3.2 The board notes that, despite the fact that the appellant's arguments under Article 123(2) EPC were only presented at oral proceedings, the same objection - albeit with a slightly different argumentation - had already been raised by the board in writing. Hence, the respondent had already had an opportunity to address it (Article 12(1)(c) RPBA). Moreover, this late-filed request not only prima facie fails to overcome the deficiencies of the main request under Article 123(2) EPC (supra) but also introduces amendments which raise new issues under Article 123(2) EPC. Indeed, it is not readily apparent where any basis is to be found for a method for identifying BSE which comprises the combination of features as claimed.

3.3 As such, the first auxiliary request is prima facie not allowable under Article 123(2) EPC and the board thus exercises its discretion under Article 13 RPBA not to admit it into the proceedings.

4. Second auxiliary request: Admissibility

4.1 This request - which consists of the set of claims as granted - was submitted during the written proceedings as a response to the objections under Articles 123(2) and 84 EPC raised in the board's communication sent under Article 15(1) RPBA.

4.2 This set of claims is broader in scope than the set of claims as maintained by the opposition division (present main request). Allowing such a claim set would thus put the opponent and sole appellant in a worse situation than if it had not filed an appeal, contrary to the principles of prohibition of reformatio in peius summarised by the Enlarged Board of Appeal in G 9/92 (OJ 1994, 875; headnote II). It follows that such a claim set can only be admitted in exceptional circumstances and following the principles developed in G 1/99 (OJ EPO 2001, 381).

G 1/99, headnote and point 15 of the reasons, states that, where the patent as maintained in amended form would otherwise have to be revoked as a direct consequence of an inadmissible amendment held allowable by the opposition division, the non-appealing patent proprietor/respondent has three possibilities for amendments: the first of these possibilities consists of the addition of further limiting features to the claim, while the last of these possibilities consists of deleting the inadmissible amendment maintained by the opposition division, within the limits of Article 123(3) EPC.

4.3 The board observes that the exceptional possibilities for amendment foreseen by G 1/99 (supra) only apply if the patent would otherwise have to be revoked, i.e. provided that, in view of the prohibition of reformatio in peius, the patent proprietor did not have any other possibility of amendment which would allow rescue of even part of the opposed patent. In the present case however such a possibility existed: the respondent could have simply deleted the alternative "bovine spongiform encephalopathy" from claim 1. Although this would have resulted in a restriction of scope, it cannot be considered unduly or inequitable for a patent proprietor who, having not appealed, cannot from the outset expect to get more than what was already maintained by the opposition division. It is clear from G 1/99 (see point 15 of the reasons) that the principle of reformatio in peius has to be respected by the boards of appeal and that any exception to this principle should be construed narrowly.

4.4 As regards the respondent's arguments based on decision T 1979/11 of 28 June 2013 it is noted that in the underlying case an amendment restricting rather than broadening the scope was apparently not available. Moreover, the broadening of scope was a reaction by the respondent/patentee to an objection by the appellant/opponent which had been raised for the first time in the statement of the grounds of appeal; the board in T 1979/11 thus concluded that it would not be equitable to allow the appellant/opponent to present a new attack and at the same time to deprive the proprietor/respondent of a means of defence (reasons 2.1). In the present case, however, there has been no new attack from the appellant but rather an objection raised by the board and then also taken up by the appellant.

4.5 The second auxiliary request is thus not admitted into the proceedings.

5. Third auxiliary request

5.1 Admissibility

The third auxiliary request was filed in due time as sixth auxiliary request with the respondent's reply to the grounds of appeal (Article 12(1)(b) and (2) RPBA), and then re-filed as second auxiliary request with the respondent's reply to the board's communication (Article 12(1)(c) RPBA) and finally re-numbered at oral proceedings. It is furthermore considered as a bona fide attempt to overcome the objections on file. The appellant has made no objections to the admission of this request into the appeal proceedings; the board also has none. The third auxiliary request is thus admitted into the proceedings.

5.2 Articles 123(2), 84, 83 and 54 EPC

All claims of this request are identical to granted claims and thus Article 84 EPC is not open for discussion. Moreover, since the patent proprietor (respondent) has not agreed to the introduction of fresh grounds of opposition, Articles 123(2) and 83 EPC, which were not invoked as grounds of opposition, are not open for discussion either (G 9/91 supra, reasons 18). Lastly, no novelty objection has been raised against these claims and the board too is satisfied that the claimed subject-matter is novel.

5.3 Inventive step

5.3.1 The claimed subject-matter is directed to methods of diagnosing BSE, which involve immunoblotting of prion (PrP)-containing samples, previously treated with proteinase K. Identification of a specific pattern of abundance of PrP glycoforms - with decreasing band intensity from the higher to the lower molecular weight glycoforms - makes it possible to distinguish BSE from other prion diseases, even in cases of BSE transmission to other species. As pointed out by the respondent, such a method is of relevance for epidemiological studies, overcoming difficulties described in the prior art (D5, page 340, right column, first four lines of "Discussion").

5.3.2 Documents D1 and D4 were considered by both parties as equally suitable starting points for the discussion of inventive step. Both documents disclose Western blotting of PrP-containing samples as a method of diagnosis for prion diseases. However, document D1 is concerned with establishing Western blot profiles for different scrapie strains (i.e. typing of scrapie), while D4 is directed at diagnosing prion diseases in general, including BSE (see abstract). And although many of D4's experimental procedures involve scrapie samples, Figure 7 of D4 is specifically directed to detection of BSE. Hence, document D4 which is directed to the same purpose as claim 1 of the third auxiliary request - namely identification of BSE infection - is the closest prior art.

5.3.3 D4 discloses Western blot mapping of disease-specific amyloid in various animal species and humans with transmissible spongiform encephalopathies (TSE), see title. The method involves treatment of the samples with proteinase K, followed by SDS-disc PAGE (electrophoresis) and then immunoblotting (page 2569, left column, second and third paragraphs). D4 further discloses that "in the immunoblot, (...), a characteristic three-band pattern in the molecular mass range 20-30 kDa can be clearly visualized" (page 2569, right column, last sentence). The difference to claim 1 is thus that a specific pattern of band intensities for BSE is not disclosed, as, in fact, D4 does not analyse differences in band intensities at all.

5.3.4 The technical problem can thus be formulated as the provision of a method for identification of infection with BSE, and the solution is the method as claimed. In view of the examples of the patent, the board is satisfied that the problem has been plausibly solved.

5.3.5 The board acknowledges that document D4 clearly teaches immunoblotting of proteinase K-treated samples as suitable for the routine diagnosis of TSE in non-experimental hosts such as sheep, cows or humans, and discusses the advantages of the method (page 2574, left column, third full paragraph). The skilled person is thus prompted by D4 to use this method for the diagnosis of TSE disease in general. By using this method, the skilled person would identify the typical three-band pattern, which is characteristic for TSE (D4, page 2569, right column, last sentence; D2, page 103, lines 9 to 12). However, there is no hint in D4 that the analysis of band intensities for the different-sized glycoforms may allow to distinguish different prion diseases, let alone that the identification of a specific 3-band pattern with decreasing intensity from the higher to the lower molecular-weight band, as in claim 1, makes it possible to distinguish BSE from other prion diseases.

5.3.6 The only document on file which provides a disclosure of the claimed band pattern in a sample of BSE is document D2: in figure 2 (a photograph of an immunoblot for PrP**(sc)), such a band pattern is apparent - by simple visual inspection - on lane C1. However, there is no recognition in D2 that this band pattern, which is not further analysed or discussed in D2, is a specific band pattern for BSE which can be used to distinguish this TSE disease from other TSE diseases. Indeed, D2 is not at all concerned with the identification of band patterns for prion diseases but instead aims at providing antisera which recognise PrP**(sc) - preferably even in the absence of a step of proteinase K treatment (D2, page 106, penultimate paragraph). The skilled person would also not be in a position to conclude, solely on the basis of D2, that such a band pattern, seen once for a sample of BSE, was reproducible and of any significance at all. Hence, even if the skilled person, seeking to develop a method for detecting BSE infection, considered the combination of D4 with D2 - which is questionable - he would not arrive at the solution to the problem.

5.3.7 Similarly, the solution is also not obvious when starting from D1. Although D1 recognises that different Western blot profiles may correspond to infection with different scrapie strains, it does not teach or suggest that Western blot profiles may also distinguish prion diseases of different origins. Again, combination with D2 would not lead to the claimed solution.

5.3.8 Claim 1 of the third auxiliary request thus involves an inventive step. The same applies to dependent claims 2 to 4.

5.3.9 Claims 5 and 6 are identical to granted claims 14 and 15 which were not part of the extent to which the patent was opposed as defined by opponent's statement under Rule 76(2)(c) EPC. This subject-matter is therefore not the subject of the opposition proceedings and consequently also not of the present appeal proceedings.