In this task, you're given a paragraph from the research paper and your task is to generate a suitable title for the research paper based on the given paper. Under 100 words is a good title length.

[EX Q]: The endoplasmic reticulum (ER) is an architecturally diverse organelle that serves as a membrane source for the replication of multiple viruses. Flaviviruses, including yellow fever virus, West Nile virus, dengue virus, and Zika virus, induce unique single-membrane ER invaginations that house the viral replication machinery 1 . Whether this virus-induced ER remodeling is vulnerable to antiviral pathways is unknown. Here, we show that flavivirus replication at the ER is targeted by the interferon (IFN) response. Through genome-scale CRISPR screening, we uncovered an antiviral mechanism mediated by a functional gene pairing between IFI6, an interferon-stimulated gene (ISG) cloned over 30 years ago 2 , and HSPA5, which encodes the ER-resident HSP70 chaperone BiP. We reveal that IFI6 is an ERlocalized integral membrane effector that is stabilized through interactions with BiP. Mechanistically, IFI6 prophylactically protects uninfected cells by preventing formation of virus-induced ER membrane invaginations. Notably, IFI6 has little effect on other mammalian RNA viruses, including the related Flaviviridae member hepatitis C virus, which replicates in double-membrane vesicles that protrude outward from the ER. These findings support a model in which the IFN response is armed with a membrane-targeted effector that discriminately blocks the establishment of virus-specific ER microenvironments required for replication. Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use:
[EX A]: A CRISPR screen identifies IFI6 as an ER-resident interferon effector that blocks flavivirus replication HHS Public Access Author manuscript

[EX Q]: The renin-angiotensin system plays an important role in the maintenance of blood pressure homeostasis. The angiotensin-converting enzyme (ACE) converts angiotensin I into angiotensin II. Angiotensin II, which binds the angiotensin II type-1 receptor (AT1R), is a potent vasoconstrictor. On a pathophysiological basis, both ACE I/D and AT1R A1166C polymorphism lead to an enhanced activity of the angiotensin II-AT1R axis, thereby possibly contributing to circulatory disturbances. A mutually facilitatory effect may be presumed between the two polymorphisms. We examined whether this synergistic effect is involved in the evolution of different types of ischemic stroke. Genetic and clinical data on 308 consecutive patients with acutely developing ischemic stroke were analyzed. A total of 272 stroke and neuroimaging alteration-free subjects served as a control group. Univariate and logistic regression statistical approaches were used. The ACE D allele combined with the AT1R 1166C allele did not yield a risk of ischemic stroke. However, the co-occurrence of the homozygous ACE D/D and at least one AT1R 1166C allele was more frequent in the ischemic stroke group than in the control group (22.4 vs 11%, p < 0.005, OR, 2.33; 95% CI, 1.46-3.7). After specific subgroup analysis, this synergistic association was even stronger for small-vessel ischemic stroke (OR, 3.44; 95% CI, 1.9-6.24; p < 0.0005). Multivariate logistic regression analysis of the data confirmed this association (adjusted OR, 3.54, 95% CI, 1.88-7.16; p < 0.0005). Our results demonstrate that ACE D/D and AT1R 1166C NeuroMolecular Medicine
[EX A]: Coexistence of Angiotensin II Type-1 Receptor A1166C and Angiotensin-Converting Enzyme D/D Polymorphism Suggests Susceptibility for Small-Vessel-Associated Ischemic Stroke

[EX Q]: Many infectious/communicable diseases (IDs) are endemic in Nepal. Until a decade and half ago, IDs were the major cause of both morbidity and mortality accounting 70% for both. However, as a result of various preventive measures implemented by both the state and non-state actors, the overall IDs have shown a changing (declining) trend. The most impressive decline has been seen in the intestinal helminth infection. Though the overall burden of IDs is decreasing, several newer infectious diseases (emerging infections) namely, dengue fever, scrub typhus, influenza (H5N1 and H1N1), and others are posing a great public health problem. On the other hand, though sporadic, outbreaks of endemic diseases together with HIV-TB coinfection and infection with drug resistance microbes during recent years have constituted a serious public health as well as medical problem. On the contrary, with the decline of IDs, noninfectious diseases (noncommunicable disease, NCD) namely, diabetes, cancer (and cancer therapy), and others are on the rise particularly in urban areas. Hence, currently Nepal is trapped in "double burden" of diseases. Risk of opportunistic infection has increased in immunocompromised person with NCD. To address the present situation, the multi-sectoral plan and strategies developed must be implemented effectively.
[EX A]:
Changing Trend of Infectious Diseases in Nepal