Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
DETAILED ACTION
Claim Status
Claims 1-15 are pending. Claims 1 and 5-6 are being examined in this application. In the response to the restriction requirement, Applicants elected the method of claim 1, SEQ ID NO: 2, wherein no pharmaceutical compound is further administered, M. Tubercolosis, macrophage, and wherein the subject is human. Claims 3-4 and 7-15 are withdrawn as being drawn to a nonelected species.
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
This rejection has been modified.
Claims 1 and 5-6 are rejected under 35 U.S.C. 103 as being unpatentable over Hare et al. (Proteomics 2015, 15, 3020-3029).
The claims are drawn to a method of increasing the cellular concentration of an Interferon Induced Protein with Tetratricopeptide repeats (IFIT) polypeptide in a cell infected with a mycobacterium, the method comprising introducing an exogenous IFIT polypeptide or an expression vector comprising a polynucleotide encoding the exogenous IFIT polypeptide into the cell, wherein the exogenous IFIT polypeptide is selected from at least one exogenous IFIT1 (SEQ ID NO: 1),IFIT2 (SEQ ID NO: 2), or IFIT3 (SEQ ID NO: 3) polypeptide, and wherein increasing the cellular concentration of the IFIT polypeptide reduces the number of viable mycobacteria in the cell.
Therefore, the only active step of the claimed method is the introduction of an exogenous IFIT polypeptide or an expression vector comprising a polynucleotide encoding the exogenous IFIT polypeptide into a cell infected with a mycobacterium
With respect to claims 1 and 5, Hare et al. teach that IFIT1, IFIT2 and IFIT3, which correspond to instantly claimed SEQ ID NOs: 1-3, increased in abundance in microparticles issued from M. tuberculosis-infected macrophages (abstract; page 3027, left column, 1st para; page 3021, left column, 3rd para; Table 1).
Hare et al. also teach that “[W]hile an essential role for ISG15 and ISGylation in anti-viral immunity has been demonstrated, the role of ISG15 in immunity to bacterial infection has largely been unexplored. A recent study, however, demonstrated that modulation of ISGylation is critical for resistance against Salmonella typhimurium and virulent M. tb” (page 3026, right column) and that “[I]nterestingly, a number of ISGylation candidates are also type I IFN inducible proteins, including the IFIT proteins, which we observed at increased abundance in the TBinf-MP” (page 3026, right column).
Hare et al. additionally teach that “[T]ype I IFN inducible proteins may have an important role in the innate immune response to M. tb” (page 3027, right column), and “[W]hile increased ifit gene expression has been observed in M. tb infection, no functional role in anti-bacterial immunity or role in MP biology has been determined” (page 3027, left column).
Hare et al. further teach that “[T]he interaction between M. tb and the host type I IFN signaling pathway is crucial in determining successful infection, and further elucidation of this pathway may yield novel therapeutic targets” (page 3028, left column).
It would have been obvious, with a reasonable expectation of success, to one of ordinary skill in the art to introduce IFIT1, IFIT2 or IFIT3 into a cell infected with M. tuberculosis because Hare et al. teach that modulation of ISGylation is critical for resistance against virulent M. tuberculosis and further teach that IFIT proteins are a number of ISGylation candidates.
One of ordinary skill in the art would have been motivated to do so because Hare et al. teach that elucidation of type I IFN signaling pathway may yield novel therapeutic targets.
Furthermore, the skilled artisan would have reasonably expected the introduction of exogenous IFIT1, IFIT2 or IFIT3 to increase the cellular concentration of IFIT1, IFIT2 or IFIT3 in a cell infected with M. tuberculosis, thus reducing the number of viable mycobacteria in said cell.
With respect to claim 6, Hare et al. teach that “[P]revious studies demonstrated that M. tuberculosis (M. tb) infection of macrophages increased the release of MPs, and these MPs induced a proinflammatory response from uninfected macrophages in vitro and in vivo following their transfer into uninfected mice (abstract).
Therefore, it would have been obvious to introduce the IFIT polypeptide into a macrophage infected with M. tuberculosis.
The skilled artisan would have reasonably expected the IFIT polypeptide to reduce the number of viable mycobacteria in cells infected with M. tuberculosis.
Response to Arguments
Applicant’s arguments filed on 6/3/2026 have been fully considered but they are not persuasive.
Applicant argues that “[T]he Examiner's reasoning conflates antiviral immunity with antibacterial immunity. Mycobacterium tuberculosis is a bacterium, not a virus. The Examiner has not explained why mechanisms that inhibit viral mRNA translation and viral replication would be expected to reduce viable bacteria. Hare's teaching that IFITs inhibit viral replication provides no basis for concluding that IFITs would reduce viable mycobacteria, as bacteria and viruses have fundamentally different structures and replication mechanisms”.
Applicant also argues that “[B]ecause IFIT proteins are type I interferon-inducible proteins, Hare's teachings suggest that increasing IFIT expression would antagonize the protective IFN-y signaling pathway, potentially worsening disease outcomes rather than providing therapeutic benefit”.
Applicant further argues that “[T]he Examiner's conclusion that one of ordinary skill in the art would have reasonably expected the introduction of exogenous IFIT polypeptides to reduce viable mycobacteria is unsupported by Hare and contradicts Hare's actual teachings. Hare proposes IFITs as "candidate biomarkers for M. tb infection." Hare, Page 3020, Abstract. This is a diagnostic application, not a therapeutic one. Hare does not teach or suggest that introducing exogenous IFIT polypeptides would have any therapeutic effect against mycobacterial infection”.
Applicant’s arguments are not persuasive.
First of all, it is noted that the fact that the inventor has recognized another advantage which would flow naturally from following the suggestion of the prior art cannot be the basis for patentability when the differences would otherwise be obvious. See Ex parte Obiaya, 227 USPQ 58, 60 (Bd. Pat. App. & Inter. 1985).
As discussed above, Hare et al. teach that “[W]hile an essential role for ISG15 and ISGylation in anti-viral immunity has been demonstrated, the role of ISG15 in immunity to bacterial infection has largely been unexplored. A recent study, however, demonstrated that modulation of ISGylation is critical for resistance against Salmonella typhimurium and virulent M. tb” (page 3026, right column) and that “[I]nterestingly, a number of ISGylation candidates are also type I IFN inducible proteins, including the IFIT proteins, which we observed at increased abundance in the TBinf-MP” (page 3026, right column).
Therefore, one of ordinary skill in the art would have been motivated, with a reasonable expectation of success, to introduce ISGylation candidates such as IFIT1, IFIT2 or IFIT3 into a cell infected with M. tuberculosis because Hare et al. teach that modulation of ISGylation is critical for resistance against virulent M. tb.
Furthermore, Applicant points to the following statement of Hare et al.:
“[T]he secretion of some mycobacterial products by virulent M. tb strains may induce type I IFN inducible genes and this may be associated with more severe disease [39]” (para bridging pages 3027-3028).
However, reference [39] (i.e. Stanley et al.; J Immunol. 2007 Mar 1;178(5):3143-52) states the following:
“[T]hese data indicate a protective role for type I IFNs during infection with M. tuberculosis”.
Thus, given the protective role for type I IFNs during infection with M. tuberculosis, one of ordinary skill in the art would have been motivated, with a reasonable expectation of success, to introduce type I IFNs such as IFIT1, IFIT2 or IFIT3 into a cell infected with M. tuberculosis.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to SERGIO COFFA whose telephone number is (571)270-3022. The examiner can normally be reached M-F: 6AM-4PM.
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If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, MELISSA FISHER can be reached at 571-270-7430. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/SERGIO COFFA Ph.D./
Primary Examiner
Art Unit 1658
/SERGIO COFFA/Primary Examiner, Art Unit 1658
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