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.

[Q]: A new species of parvovirus, tentatively named human bocavirus 4 (HBoV4), was genetically characterized. Among 641 feces samples obtained from children and adults, the most commonly detected bocavirus species were, in descending order, HBoV2, HBoV3, HBoV4, and HBoV1, with an HBoV2 prevalence of 21% and 26% in Nigerian and Tunisian children, respectively. HBoV3 or HBoV4 species were found in 12 of 192 patients with non-polio acute flaccid paralysis in Tunisia and Nigeria and 0 of 96 healthy Tunisian contacts (P p ). Evidence of extensive recombination at the NP1 and VP1 gene boundary between and within bocavirus .01 species was found. The high degree of genetic diversity seen among the human bocaviruses found in feces specimens, relative to the highly homogeneous HBoV1, suggest that this worldwide-distributed respiratory pathogen may have recently evolved from an enteric bocavirus after acquiring an expanded tropism favoring the respiratory tract. Elucidating the possible role of the newly identified enteric bocaviruses in human diseases, including acute flaccid paralysis and diarrhea, will require further epidemiological studies. Parvoviruses are small, non-lipid-enveloped, environmentally resistant viral particles with single-stranded linear DNA genomes that frequently infect animals through the fecal-oral route [1] . Parvoviruses can cause numerous symptoms in animals, including enteritis, panleukopenia, hepatitis, erythrocyte aplasia, and cerebellar ataxia [1]. Efficacious vaccines against animal parvovirus infections are widely employed [2] [3] [4] . Following the identification of the human parvovirus
[A]: Human Bocaviruses Are Highly Diverse, Dispersed, Recombination Prone, and Prevalent in Enteric Infections


[Q]: Hepatitis C virus (HCV) infects more than 2 % of the world population with highest prevalence in parts of Africa and Asia. Past standard of care using interferon α and ribavirin had adverse effects and showed modest efficacy for some HCV genotypes spurring the development of direct acting antivirals (DAAs). Such DAAs target viral proteins and are thus better tolerated but they suffer from emergence of vial resistance. Furthermore, DAAs are often HCV genotype specific. Novel drug candidates targeting host factors required for HCV propagation, so called host-targeting antivirals (HTAs), promise to overcome both caveats. The genetic barrier to resistance is usually considered to be high for HTAs and all HCV genotypes presumably use the same host factors. Recent data, however, challenge these assumptions, at least for some HTAs. Here, we highlight the most important hosttargeting strategies against hepatitis C and critically discuss their opportunities and risks.
[A]: Opportunities and Risks of Host-targeting Antiviral Strategies for Hepatitis C


[Q]: Highlights d N 1 -2 0 O-methylation is crucial to block RIG-I activation by viral and self RNA d Self-RNA exclusion is singularly governed by the conserved H830 in RIG-I d H830A alteration leads to indiscriminate recognition of endogenous RNA by RIG-I d Cellular N 1 -2 0 O-methyltransferase knockdown renders endogenous RNA stimulatory SUMMARY The cytosolic helicase retinoic acid-inducible gene-I (RIG-I) initiates immune responses to most RNA viruses by detecting viral 5 0 -triphosphorylated RNA (pppRNA). Although endogenous mRNA is also 5 0 -triphosphorylated, backbone modifications and the 5 0 -ppp-linked methylguanosine ( m7 G) cap prevent immunorecognition. Here we show that the methylation status of endogenous capped mRNA at the 5 0 -terminal nucleotide (N 1 ) was crucial to prevent RIG-I activation. Moreover, we identified a single conserved amino acid (H830) in the RIG-I RNA binding pocket as the mediator of steric exclusion of N 1 -2 0 O-methylated RNA. H830A alteration (RIG-I(H830A)) restored binding of N 1 -2 0 O-methylated pppRNA. Consequently, endogenous mRNA activated the RIG-I(H830A) mutant but not wild-type RIG-I. Similarly, knockdown of the endogenous N 1 -2 0 O-methyltransferase led to considerable RIG-I stimulation in the absence of exogenous stimuli. Studies involving yellow-fever-virus-encoded 2 0 O-methyltransferase and RIG-I(H830A) revealed that viruses exploit this mechanism to escape RIG-I. Our data reveal a new role for cap N 1 -2 0 O-methylation in RIG-I tolerance of self-RNA.
[A]:
A Conserved Histidine in the RNA Sensor RIG-I Controls Immune Tolerance to N 1 -2 0 O-Methylated Self RNA Article A Conserved Histidine in the RNA Sensor RIG-I Controls Immune Tolerance to N 1 -2 0 O-Methylated Self RNA