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 .
Application Status
The action is written in response to applicant’s correspondence received on 8/13/2026. Claims 1-37 are currently pending in the instant application.
Priority
The instant application claims priority to US Provisional application 63/384,541, with an effective filing date of 11/21/2022.
Election/Restriction
Applicant's election with traverse of the inventions of Group II (claims 9-14, drawn to a method to increase influenza virus yield in cells) in the reply filed on 8/13/2026 is acknowledged.
Applicant further elects SEQ ID NO: 1.
The traversal is on the grounds that a method of increasing influenza virus yield, a method to detect influenza virus in a sample, a method to prevent, inhibit, or treat influenza virus infection in an avian or mammal, or a method to screen for compounds by contacting the cell with a nucleic acid vector comprising a polypeptide encoded by one of SEQ ID NOs: 1-36 or 74-91 or a portion thereof, is related. This is not found persuasive because though they are related to an influenza virus, they require different fields of search that would impart a search burden, evidenced by different CPC classifications. As one method is directed towards increasing virus yield or decreasing viral yield in a subject, and another is a method of screening for host factors, one of reasonable skill in the art would expect these methods to be directed towards non-related outcomes or separate method steps.
Furthermore, regarding the election of species for SEQ ID NO: 1, a complete and comprehensive search of all SEQ ID NOs: 1-36 or 74-91 would require an immense search burden as each sequence would require an individual search. Furthermore, art that applies to one SEQ ID NO would likely not apply to another. This is evidenced by SEQ ID NO: 1 which refers to a sodium/hydrogen exchanger protein, where SEQ ID NO: 6 refers to an olfactory receptor, which is a completely different class of enzymes.
The requirement is still deemed proper and is therefore made FINAL.
Claims 1-8 and 15-37 are withdrawn from further consideration pursuant to 37 CFR 1.142(b), as being drawn to a nonelected invention, there being no allowable generic or linking claim. Applicant timely traversed the restriction (election) requirement in the reply filed on 8/13/2026.
Claims 9-14 are currently under examination of the merits.
Drawings
The drawings are objected to under 37 CFR 1.83(a) because they fail to show “changes in the population over sequential passages” (Fig. 7) as described in the specification. Any structural detail that is essential for a proper understanding of the disclosed invention should be shown in the drawing. MPEP § 608.02(d). Corrected drawing sheets in compliance with 37 CFR 1.121(d) are required in reply to the Office action to avoid abandonment of the application. Any amended replacement drawing sheet should include all of the figures appearing on the immediate prior version of the sheet, even if only one figure is being amended. The figure or figure number of an amended drawing should not be labeled as “amended.” If a drawing figure is to be canceled, the appropriate figure must be removed from the replacement sheet, and where necessary, the remaining figures must be renumbered and appropriate changes made to the brief description of the several views of the drawings for consistency. Additional replacement sheets may be necessary to show the renumbering of the remaining figures. Each drawing sheet submitted after the filing date of an application must be labeled in the top margin as either “Replacement Sheet” or “New Sheet” pursuant to 37 CFR 1.121(d). If the changes are not accepted by the examiner, the applicant will be notified and informed of any required corrective action in the next Office action. The objection to the drawings will not be held in abeyance.
Regarding Fig. 7, the drawings show what appears to be figure legends with no identifying characteristics for the changes in population over sequential passages (shown below). It is unclear what these legends, or identifying characteristics refer to, leaving the drawing unclear. The specification does not provide any guidance or descriptive elements.
PNG
media_image1.png
108
686
media_image1.png
Greyscale
The drawings are objected to because Figs. 14A-D, 14F, 14H, 15A-B, 16A, 16C, 16E-F, 18A-H, 19E, 19G, 20A-E, 20G, 21A, 21C, 22B-C, 23A-C, 23F-23G, and 24C all have elements, or boxes, without any subsequent material or identifying characteristics. Corrected drawing sheets in compliance with 37 CFR 1.121(d) are required in reply to the Office action to avoid abandonment of the application. Any amended replacement drawing sheet should include all of the figures appearing on the immediate prior version of the sheet, even if only one figure is being amended. The figure or figure number of an amended drawing should not be labeled as “amended.” If a drawing figure is to be canceled, the appropriate figure must be removed from the replacement sheet, and where necessary, the remaining figures must be renumbered and appropriate changes made to the brief description of the several views of the drawings for consistency. Additional replacement sheets may be necessary to show the renumbering of the remaining figures. Each drawing sheet submitted after the filing date of an application must be labeled in the top margin as either “Replacement Sheet” or “New Sheet” pursuant to 37 CFR 1.121(d). If the changes are not accepted by the examiner, the applicant will be notified and informed of any required corrective action in the next Office action. The objection to the drawings will not be held in abeyance.
Claim Objections
Claim 9 is objected to because of the following informalities: Claim 9 recites “comprising any one of the claims 1 or…”. Claim 9 is recited to be dependent on a non-elected independent claim 1. Claim 9 should be re-written in independent form to incorporate the limitations of claim 1. Appropriate correction is required.
Claim Rejections - 35 USC § 112
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Written Description
Claims 9-14 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention.
The factors to be considered when analyzing claims for compliance with the written description requirement include: (A) actual reduction to practice; (B) disclosure of drawings or structural chemical formulas; (C) sufficient relevant identifying characteristics (e.g., complete structure, partial structure, physical and/or chemical properties, structure/function correlation); (D) level of skill and knowledge in the art; and (E) predictability in the art.
Each of the factors (A)-(E) listed above is analyzed below:
Actual Reduction to Practice
For actual reduction to practice, applicant discloses Figs. 17-24, which employes methods to determine the activity of identified factors employing the 3’-5’ DNA exonuclease TREX1 as an example. Figs. 18 A and B show multiple TRIPC viruses with distinct targeting sequences activate TREX1 and Fig. 18C where TREX1 activation enhances viral growth. Furthermore, Fig. 19D shows where transient expression of TREX1 boosts viral replication.
Applicant does not provide any reduction to practice or show the structure-function correlation of a construct comprising a polynucleotide encoding any of SEQ ID NOs: 1-36 or 74-91 to increase viral yield, or a polypeptide of at least 80% identity of SEQ ID NOs: 1-36 and 74-91, or a fragment thereof. It is important to note that TREX1 is not one of the claimed SEQ ID NOs, therefore, the characterized activity and use of TREX1 does not apply to the claimed SEQ ID NOs.
Disclosure of Drawings or Structural Chemical Formulas
Applicant discloses Fig. 16E-16G, which show the results of 3 screens using MAGeCK to look for pro-viral host factors in the human genome. Applicants show that SLC9C1 is one of the top candidates, exhibiting the most predicted fold-change across 3 replicate screening procedures.
Sufficient Relevant Identifying Characteristics
Applicant discloses the structure of a nucleic acid vector to comprise a promoter (such as a viral promoter) linked to an open reading frame encoding a polypeptide having at least 80% amino acid sequence identity to one of the SEQ ID NOs: 1-36 or 74-91. Applicant further discloses wherein the promoter can be a viral vector and the vector (see page 2 line 21 of the instant specification) and where the cell is contacted with the vector or polypeptide before or after contacting cells with the influenza virus (see page 3, line 18).
Regarding at least 80% identity of a polypeptide to any one of SEQ ID NOs: 1-36 and 74-91, or an active fragment thereof, applicant does not disclose what specific amino acid sequences are required, what sequences can be modified, or any length limitations to the fragment, only that it is active.
Applicant discloses Fig. 17D which shows that host factor screening methods identified proteins related, but not limited to, hydrolase activity, carbohydrate derivative binding, transporter activity, transferase activity, transmembrane transporter activity, signaling receptor activity, amongst others.
As the instant claims are directed to a method of increasing viral yield, applicant does not show where a construct comprising a polypeptide encoded by SEQ ID NOs: 1-36 or 74-91 or an active fragment thereof, have been administered to a host cell in order to increase influenza viral yield or the claimed method recited in claim 9.
Level of Skill and Knowledge in the Art
The level of skill and knowledge in Art is high. A skilled artisan would require knowledge about modifying viral replication through modulating host factor expression within a host cell.
Predictability in the Art
The art is highly unpredictable. A skilled artisan would recognize that methods of screening for host factors is known in the art as evidenced by Han et al. (Genome-wide CRISPR/Cas9 Screen Identifies Host Factors Essential for Influenza Virus Replication, Cell Reports, Volume 23, Issue 2, Pgs. 596-607, published 4/10/2018) and Mehle et al. (A Host of Factors Regulating Influenza Virus Replication, Viruses, Volume 2, Issue 2, pgs. 566-573, published 1/25/2010). Han discloses the use of genome-wide CRISPR knockout (GeCKO) screening to investigate host factors associated with viral replication (see introduction). Han further discloses that using MAGeCK analysis to identify positively selected genes at Round 2 and Round 5 showed the enrichment of 798 genes at Rd2, with 161 genes represented by two or more sgRNAs and 637 genes represented by a single sgRNA, where by Rd5, 501 genes were enriched, where only 16 were represented by sgRNA by two or more sgRNAs. The decrease in the number of genes represented by multiple sgRNAs between Rd2 and Rd5 suggests that stringent H5N1 selection results in the preferential enrichment of individual sgRNAs (see section titled “Identification of Genes Enriched during Sequential H5N1 Selection). Han identified and tested SLC35A1, which was one of the highest enriched genes using the GeCKO method, which demonstrated a ~50% decrease in H1N1 infection. However, JAK2 was another host factor identified by Han which was previously implicated in IAV entry. However, in JAK2 KOs, Han observed no defects in flu VLP entry yet decreased genome replication at 6 hpi. It is possible that increased antiviral gene expression may suppress IAV genome replication in JAK2 KOs. Therefore, studies are necessary to delineate the role of JAK2 in IAV replication (see discussion). Therefore, Han shows that merely screening is not enough to fully determine the role of a host factor in viral replication.
Mehle et al. (A Host of Factors Regulating Influenza Virus Replication, Viruses, Volume 2, Issue 2, pgs. 566-573, published 1/25/2010) teaches the use of genome-wide siRNA silencing screens to characterize host proteins involved in influenza virus infection (see abstract). Mehle further teaches where the screens have provided an abundance, maybe even an overabundance, of likely influenza virus host factors. Out of the 1539 total hits obtained in 5 screens, 1417 are unique. However, only about 8% of identified genes is common to at least two screens and non-gene was shared by all 5 screens. Mehle discloses that such differences in screening, infection assays and data analysis almost certainly limit the type of factors that can be identified and the coincidence of factors between screens. The possibility that the screens might also possess high false positive and false negative rates which would contribute to the large number of genes identified and low overlap between data sets cannot be eliminated.
To conclude, the unpredictable nature of the invention resides in both whether the screens can accurately and consistently identify host factors, which is uncertain as evidenced by Han and Mehle, and whether modulation of these host factors can increase viral yield within a host cell. As applicant does not disclose a reduction to practice or structure-function correlation of a construct comprising a nucleic acid encoding a polypeptide of any of SEQ ID NOs: 1-36 or 74-91, or a polypeptide with at least 80% identity, or an active fragment for the purpose of a method to increase viral yield, one skilled in the art cannot assess that the inventor had full possession of the claimed invention at the time of filing. Applicants only shows practice of a single host factor, TREX1, in modulating viral production, which is not even a claimed SEQ ID NO. Furthermore, TREX1 is a 3’-5’ DNA exonuclease where SLC9C1 (SEQ ID NO: 1) is drawn to a sodium/hydrogen exchanger polypeptide, which is in an entirely different class of its own.
In view of the foregoing, claims 9-14 are rejected under 35 U.S.C. 112(a) as failing to comply with the written description requirement.
Enablement
Claims 9-14 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the enablement requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to enable one skilled in the art to which it pertains, or with which it is most nearly connected, to make and/or use the invention.
The test of enablement is whether one skilled in the art could make and use the claimed invention from the disclosures in the specification coupled with information known in the art without undue experimentation (United States vs Telectronics., 8 USPQ2d 1217 (Fed. Cir. 1988)). Whether undue experimentation is needed is not based upon a single factor but rather is a conclusion reached by weighing many factors. These factors were outlined in Ex parte Forman, 230 USPQ 546 (Bd. Pat. App. & Inter. 1986) and again in In re Wands, 8 USPQ2d 1400 (Fed. Cir. 1988), and the most relevant Wands factors are indicated below:
As stated in MPEP §2164.01(a), “there are many factors to consider when determining whether there is sufficient evidence to support a determination that a disclosure does not satisfy the enablement requirement and whether any experimentation is ‘undue’.” These factors include, but are not limited to:
The nature of the invention;
The breadth of the claims;
The state of the prior art;
The level of skill in the art;
The level of predictability in the art;
The amount of direction provided by the inventor;
The presence or absence of working examples;
The quantity of experimentation necessarily needed to make or use the invention based on the disclosure.
See In re Wands USPQ 2d 1400 (CAFC 1988).
Further MPEP §2164.01(c) recites, “When a compound or composition claim is limited by a particular use, enablement of that claim should be evaluated based on that limitation. See In re Vaeck, 947 F.2d 488, 495, 20 USPQ2d 1438, 1444 (Fed. Cir. 1991) (claiming a chimeric gene capable of being expressed in any cyanobacterium and thus defining the claimed gene by its use).”
Nature of the Invention
The nature of the invention is drawn to a method of increasing the yield of influenza virus within a host cell through modulation of host factors that impact viral replication.
Breadth of the Claims
The breadth of the claims is narrow. Applicant fully discloses the intended effect or method in the claim, being increasing influenza virus yield, by contacting the influenza virus and cells comprising a vector or contacting cells with a polypeptide that has at least 80% identity to any one of SEQ ID NOs: 1-36 or 74-91. Looking to the specification for guidance, SEQ ID NOs: 1-36 or 74-91 are drawn towards pro-viral host factors.
The State of the Prior Art
The state of the prior art does not provide any evidence that SLC9C1 serves as a pro-viral host factor that is capable of increasing viral yield within a host cell when administered as a polypeptide. Looking towards post-filing date art, Examiner identifies inventors own published work, King et al. (Pathogen-driven CRISPR screens identify TREX1 as a regulator of DNA self-sensing during influenza virus infection, Cell Host Microbe, Volume 31, Issue 9, pgs. 1552-1567, published 8/30/2023), where King discloses SLC9C1 was the top-ranked candidate from their screen, which was surprising because the gene is not normally expressed in lung cells. King discloses while the mechanism by which SLC9C1 affects IAV replication is unclear, its appearance as a top candidate in all three independent screens suggest a strong impact on viral replication and raises the possibility of previously unappreciated that impact virion production. A potential limitation of the screen and the interpretation of the results invovlves the CRISPRa/I system where efficiency of transcriptional control is affected by sgRNA, some of which are more potentat than others (see discussion). The prior art of Han and Mehle, as disclosed above, further indicates the unpredictable nature of screening for host factors. This is evidenced by Han where Han identified and tested SLC35A1, which was one of the highest enriched genes using the GeCKO method, which demonstrated a ~50% decrease in H1N1 infection. However, JAK2 was another host factor identified by Han which was previously implicated in IAV entry. However, in JAK2 KOs, Han observed no defects in flu VLP entry yet decreased genome replication at 6 hpi. It is possible that increased antiviral gene expression may suppress IAV genome replication in JAK2 KOs. Therefore, studies are necessary to delineate the role of JAK2 in IAV replication (see discussion). Therefore, Han shows that merely screening is not enough to fully determine the role of a host factor in viral replication.
The Level of Skill in the Art
The level of skill and knowledge in Art is high. A skilled artisan would require knowledge about modifying viral replication through modulating host factor expression within a host cell.
The Level of Predictability in the Art
The art is highly unpredictable. A skilled artisan would recognize that methods of screening for host factors is known in the art as evidenced by Han et al. (Genome-wide CRISPR/Cas9 Screen Identifies Host Factors Essential for Influenza Virus Replication, Cell Reports, Volume 23, Issue 2, Pgs. 596-607, published 4/10/2018) and Mehle et al. (A Host of Factors Regulating Influenza Virus Replication, Viruses, Volume 2, Issue 2, pgs. 566-573, published 1/25/2010). Han discloses the use of genome-wide CRISPR knockout (GeCKO) screening to investigate host factors associated with viral replication (see introduction). Han further discloses that using MAGeCK analysis to identify positively selected genes at Round 2 and Round 5 showed the enrichment of 798 genes at Rd2, with 161 genes represented by two or more sgRNAs and 637 genes represented by a single sgRNA, where by Rd5, 501 genes were enriched, where only 16 were represented by sgRNA by two or more sgRNAs. The decrease in the number of genes represented by multiple sgRNAs between Rd2 and Rd5 suggests that stringent H5N1 selection results in the preferential enrichment of individual sgRNAs (see section titled “Identification of Genes Enriched during Sequential H5N1 Selection).
Mehle teaches the use of genome-wide siRNA silencing screens to characterize host proteins involved in influenza virus infection (see abstract). Mehle further teaches where the screens have provided an abundance, maybe even an overabundance, of likely influenza virus host factors. Out of the 1539 total hits obtained in 5 screens, 1417 are unique. However, only about 8% of identified genes is common to at least two screens and non-gene was shared by all 5 screens. Mehle discloses that such differences in screening, infection assays and data analysis almost certainly limit the type of factors that can be identified and the coincidence of factors between screens. The possibility that the screens might also possess high false positive and false negative rates which would contribute to the large number of genes identified and low overlap between data sets cannot be eliminated.
The Amount of Direction Provided by the Inventor
Applicant discloses the structure of a nucleic acid vector to comprise a promoter (such as a viral promoter) linked to an open reading frame encoding a polypeptide having at least 80% amino acid sequence identity to one of the SEQ ID NOs: 1-36 or 74-91. Applicant further discloses wherein the promoter can be a viral vector and the vector (see page 2 line 21 of the instant specification) and where the cell is contacted with the vector or polypeptide before or after contacting cells with the influenza virus (see page 3, line 18).
Furthermore, applicant only discloses that an amino acid sequence of 80% identity to any of SEQ ID NOs: 1-36, or 74-91, or a portion with activity thereof may be used in the construct. However, applicant does not provide structural limitations, such as definition any core catalytic regions or essential structures that would constitute “a portion” thereof or required amino acids that constitute at least 80% of an active polypetide.
The Presence or Absence of Working Examples
For actual reduction to practice, applicant discloses Figs. 17-24, which employes methods to determine the activity of identified factors employing the 3’-5’ DNA exonuclease TREX1 as an example. Figs. 18 A and B show multiple TRIPC viruses with distinct targeting sequences activate TREX1 and Fig. 18C where TREX1 activation enhances viral growth.
Furthermore, Fig. 19D shows where transient expression of TREX1 boosts viral replication.
Applicant does not provide any reduction to practice or show the structure-function correlation of a construct comprising a polynucleotide encoding any of SEQ ID NOs: 1-36 or 74-91 to increase viral yield, as TREX1 is not one of the claimed SEQ ID NOs.
The quantity of experimentation necessarily needed to make or use the invention based on the disclosure.
The quantity of undue experimentation is high. A skilled artisan would need to test all host factors, encoded by any one of SEQ ID NOs: 1-36 and 74-91, or a polypeptide of 80% identity with the same activity, or a fragment thereof with activity, and determine whether the polypeptide is capable of increasing influenza virus yield in a host cell.
Conclusion of 35 U.S.C. 112(a) Enablement Analysis
After applying the Wands factors and analysis to claims 9-14, taking into consideration the factors outlined above, it is concluded that the specification is not enabled for a polypeptide comprising SEQ ID NO: 1-36 and 74-91, specifically the elected SEQ ID NO: 1, to be contacted with a cell and influenza virus, in order to increase virus production. While the state of the art discloses the discovery of host factors that modulate viral replication is very well known, as evidenced by prior filing date art of Han and Mehle, all the arts show that the screening method itself is unpredictable and can yield false positives. Even inventors post filing date art, which specifically discloses SLC9C1 as a “top-ranked” candidate, did not establish the mechanism by which SLC9C1 affects IAV replication nor does it test a construct with a SLC9C1 polypeptide, or a fragment thereof, for use in a method of increasing viral yield. Furthermore, the post filing art goes to explain sgRNA efficiency is a key factor and potential limitation of the screen implemented, further adding to the unpredictable nature of the art.
Absent evidence to the contrary and the lack of working examples that correspond to SEQ ID NO: 1-36 or 74-91, or a portion thereof, claims 9-14 are rejected under 35 U.S.C. 112(a) for failing to disclose sufficient information to enable a person of skill in the art to use the invention commensurate in scope with these claims.
Indefiniteness
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claims 9 and 11 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Regarding claim 9, the instant claim recites “cells comprising the vector of anyone of claims 1 or contacting the cells with…”. As written, claim 9 depends on a vector that can be selected from a plurality of claims, as indicated by “claims”. It is unclear whether claim 9 depends on vectors comprising a polypeptide recited in claim 1 or another unrecited claim.
Furthermore, claim 9 recites “a method…and collecting progeny influenza virus”. It is unclear how “collecting progeny influenza virus” relates to the claimed “method to increase influenza virus yield in cells” and it is also unclear whether an additional method step relating to the increasing influenza virus yield in cells is omitted.
Claim 11 recites a registered trademark (PER.C6® cells). Under MPEP § 2173.05(u), a trademark or trade name is used to identify a source of goods and is not the name of the goods themselves. Thus, a trademark or trade name does not define or describe the goods associated with the trademark or trade name.
Improper Markush Groups
Claim 9 is rejected on the basis that it contains an improper Markush grouping of alternatives. See In re Harnisch, 631 F.2d 716, 721-22 (CCPA 1980) and Ex parte Hozumi, 3 USPQ2d 1059, 1060 (Bd. Pat. App. & Int. 1984). A Markush grouping is proper if the alternatives defined by the Markush group (i.e., alternatives from which a selection is to be made in the context of a combination or process, or alternative chemical compounds as a whole) share a “single structural similarity” and a common use. A Markush grouping meets these requirements in two situations. First, a Markush grouping is proper if the alternatives are all members of the same recognized physical or chemical class or the same art-recognized class, and are disclosed in the specification or known in the art to be functionally equivalent and have a common use. Second, where a Markush grouping describes alternative chemical compounds, whether by words or chemical formulas, and the alternatives do not belong to a recognized class as set forth above, the members of the Markush grouping may be considered to share a “single structural similarity” and common use where the alternatives share both a substantial structural feature and a common use that flows from the substantial structural feature. See MPEP § 2117.
The Markush grouping of claim is improper because the alternatives defined by the Markush grouping do not share both a single structural similarity and a common use for the following reasons:
Claim 9 recites a polypeptide having at least 80% amino acid sequence identity to one of SEQ ID NOs: 1-36 or 74-91. Looking towards the specification for guidance, SEQ ID NOs: 1-36 and 74-91 are directed to different genes or host factors, each with unique amino acid sequences and no common-core structure. This is further evidenced by the varying sequence length as shown in the sequence listings. While applicants claim a related use of modulating the expression or production of influenza virus within a cell, this relationship is not established from a substantial structural feature, such as a common core sequence that is present amongst all the species claimed.
To overcome this rejection, Applicant may set forth each alternative (or grouping of patentably indistinct alternatives) within an improper Markush grouping in a series of independent or dependent claims and/or present convincing arguments that the group members recited in the alternative within a single claim in fact share a single structural similarity as well as a common use.
Conclusion
No claims are allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to DAVID YU whose telephone number is (571)272-1118. The examiner can normally be reached Monday-Friday 7:30 am -5 pm.
Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Ram Shukla can be reached at 571-272-0735. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
Information regarding the status of published or unpublished applications may be obtained from Patent Center. Unpublished application information in Patent Center is available to registered users. To file and manage patent submissions in Patent Center, visit: https://patentcenter.uspto.gov. Visit https://www.uspto.gov/patents/apply/patent-center for more information about Patent Center and https://www.uspto.gov/patents/docx for information about filing in DOCX format. For additional questions, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000.
/D.T.Y./Examiner, Art Unit 1635
/RAM R SHUKLA/Supervisory Patent Examiner, Art Unit 1635
Prosecution Insights