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 and 3-15 are pending. Claim 2 has been canceled. Claim 1 has been amended. 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 Claims 3-4 and 7-15 are withdrawn as being drawn to a nonelected species.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 is maintained.
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).
With respect to claims 1 and 5, Hare et al. teach that IFIT1, IFIT2 and IFIT3 increased in abundance in microparticles issued from M. tuberculosis-infected macrophages (abstract; page 3021, left column, 3rd para; Table 1).
Please note that IFIT1-3 correspond to instantly claimed SEQ ID NOs: 1-3 (see page 3027, left column, 1st para).
Hare et al. also 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, 1st para).
Hare et al. further teach that “[I]FITs mediate antiviral immunity by inhibiting viral mRNA translation through multiple steps or by sequestering viral RNA, resulting in the inhibition of viral replication” (page 3027, left column, 1st para).
It would have been obvious to one of ordinary skill in the art to use exogenous IFIT1, IFIT2 or IFIT3 as a treatment against mycobacterial infection because Hare et al. teach that IFIT1, IFIT2 and IFIT3 increased in abundance in microparticles issued from M. tuberculosis-infected macrophages.
One of ordinary skill in the art would have reasonably expected the introduction of exogenous IFIT1, IFIT2 or IFIT3 to increase the cellular concentration of IFIT1, IFIT2 or IFIT3, thus reducing the number of viable mycobacteria in cells infected with a mycobacterium.
With respect to claim 6, Hare et al. teach that “[P]revious studies demonstrated that Mycobacterium 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 Mycobacterium tuberculosis.
The skilled artisan would have reasonably expected the IFIT polypeptide to reduce the number of viable mycobacteria in cells infected with Mycobacterium tuberculosis.
Response to Arguments
Applicant’s arguments filed on 11/17/2025 have been fully considered but they are not persuasive.
Applicant argues that “[t]he Examiner's reasoning contains a critical gap in logic. The mere observation that IFIT proteins increased in abundance in microparticles from infected macrophages does not provide any teaching, suggestion, or motivation to introduce exogenous IFIT polypeptides as a therapeutic intervention. The Examiner has failed to establish that the increased abundance of IFIT proteins in microparticles correlates with or suggests therapeutic efficacy when introduced exogenously. Furthermore, the Examiner's conclusion that one of ordinary skill in the art would have reasonably expected exogenous IFIT introduction to reduce viable mycobacteria is unsupported speculation that lacks any factual basis in the cited reference”.
Applicant also argues that “[H]are does not teach or suggest that introducing exogenous IFIT polypeptides would have any therapeutic effect against mycobacterial infection, nor does it provide any guidance regarding the specific method steps recited in Claim 1, including the introduction of exogenous IFIT polypeptides or expression vectors into infected cells. The Examiner's analysis improperly relies on hindsight reconstruction and fails to demonstrate that the claimed method would have been obvious to one of ordinary skill in the art at the time of the invention”.
Applicant’s arguments are not persuasive.
Hare et al. state 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, 1st para).
Therefore, it is clear that the teachings Hare et al. provide a motivation to introduce exogenous IFIT polypeptides as a therapeutic intervention.
Furthermore, Hare et al. teach that “[I]FITs mediate antiviral immunity by inhibiting viral mRNA translation through multiple steps or by sequestering viral RNA, resulting in the inhibition of viral replication” (page 3027, left column, 1st para).
Thus, once again, the teachings of Hare et al. provide a clear motivation to introduce exogenous IFIT polypeptides into a macrophage infected with Mycobacterium tuberculosis.
For the reasons stated above the rejection is maintained.
Conclusion
THIS ACTION IS MADE FINAL. Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
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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/SERGIO COFFA Ph.D./
Primary Examiner
Art Unit 1658
/SERGIO COFFA/Primary Examiner, Art Unit 1658