instruction:
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.
question:
ARTICLES We synthesized three overlapping 19-amino-acid peptides spanning the F binding domain of RhoA (amino acids 67-110) and used these to study the effect of peptides on virus-induced syncytium formation. Pretreatment of virus inoculum with the RhoA 77-95 peptide completely blocked plaque formation, whereas pretreatment with RhoA 87-105 did not have any effect on the plaque formation relative to media-treated controls (Fig. 1) . The RhoA 67-85 peptide did not block RSV-induced syncytium forma- by reduction of peak titer by 2 log 10 in RSV-infected mice. These findings indicate that the interaction between these two paramyxovirus fusion proteins and RhoA is an important target for new antiviral strategies.
answer:
A RhoA-derived peptide inhibits syncytium formation induced by respiratory syncytial virus and parainfluenza virus type 3

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Ramsay Hunt syndrome (RHS) is characterized by varicella zoster virus (VZV) infection in the geniculate ganglion of the facial nerve. It typically presents with ipsilateral facial palsy and vesicles in the external auditory canal [1] . Recognizing atypical clinical manifestations of RHS, though not frequently reported, is of clinical importance for clinicians. For instance, RHS without vesicles, condition known as zoster sine herpete [2] , is difficult to distinguish itself from Bell's palsy. Although the vestibulocochlear nerve is frequently co-involved during the course of RHS, multiple lower cranial nerve involvement has rarely been described in the literature [5] [6] [7] [8] [9] [10] [11] [12] . Additionally, laryngitis due to VZV associated with RHS is not a well-recognized clinical entity. We herein report a case of Ramsay Hunt syndrome with zoster pharyngitis involving multiple lower cranial nerves. A 66-year-old woman with a history of hypertension was hospitalized because of progressive dizziness, right-side facial weakness and dysphagia. The patient was in her usual state of health until 6 days before admission, when sore throat and odynophagia developed, associated with subjective fevers and anorexia. Two days before admission, the patient reported dizziness, right-side facial weakness associated with pain radiating to the right ear, and dysphagia. The patient denied headache, photophobia, neck stiffness, nausea or vomiting. On the morning of admission, the patient developed right-side tinnitus, unsteady gait and inability to close the right eye. On physical examination, the patient appeared to be in mild distress. The temperature was 101.8 8F, blood pressure 176/93 mm Hg, pulse 102 beats per minute, respirations 20 breaths per minute and oxygen saturation 97% on room air. Her heart sounds were regular without murmurs and her lungs were clear to auscultation. On otologic examination, a few vesicles were observed in the external auditory canal of the right ear with a normal tympanic membrane. Neurological examination revealed peripheral facial nerve palsy (VII), with involvement of the left vestibulocochlear nerve (VIII), glossopharyngeal nerve (IX) and vagus nerve (X) ( Table 1) . Spinal accessory nerve (XI) and hypoglossal nerve (XII) were intact. Flexible laryngoscopic examination revealed erythema and erosive lesions on the right side of the epiglottis and arytenoid. There was an asymmetry of the soft palate. A biopsy of the erosive lesions was not performed. A non-contrast computed tomography of the head and temporal bone revealed no abnormalities. Ramsay Hunt syndrome with laryngitis due to varicella zoster virus was suspected and the patient was started on acyclovir and steroid therapy. After the completion of a 7-day course of the combination therapy, the patient's neurological symptoms improved except for the facial nerve palsy. Healed erosions on the IDCases 2 (2015) 47-48 A B S T R A C T Ramsay Hunt syndrome is characterized by varicella zoster virus infection affecting the geniculate ganglion of the facial nerve. It typically presents with vesicles in the external auditory canal associated with auricular pain and peripheral facial nerve paralysis. Although vestibulocochlear nerve is frequently co-involved during the course of Ramsay Hunt syndrome, multiple lower cranial nerve involvement has rarely been described in the literature. In addition, laryngitis due to varicella zoster virus is a diagnostic challenge due to its unfamiliarity among clinicians. We report a case of Ramsay Hunt syndrome with laryngitis involving multiple lower cranial nerves.
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Ramsay Hunt syndrome and zoster laryngitis with multiple cranial nerve involvement-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/)

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Viral envelope glycoproteins are oligomeric and the quaternary structure is critical for their membrane fusion activity. Typically the transmembrane glycoproteins of class I fusion proteins contain the oligomerization domains and the surface glycoproteins (SU) are monomeric. However, it has been previously demonstrated [J. Biol. Chem. 277 (2002) 19727] that the SU of a murine hepatitis coronavirus (MHV) forms dimers, the dimerization domain overlaps the receptor-binding domain (RBD) and that this dimeric state is important for binding to receptor molecules that initiates entry into cells. We have previously expressed various soluble fragments of the SARS-CoV SU and identified stably folded fragments (residues 272-537) that contain the RBD [Biochem. Biophys. Res. Commun. 312 (2003) 1159]. Here, we further characterize these and other fragments in an attempt to identify possible dimerization domains and their role for membrane fusion. We demonstrate that the SU and a shorter 260-amino acid N-terminal fragment (residues 17-276), which folds independently, form dimers. In contrast to the previously characterized MHV SU dimerization, this fragment is upstream and distinct from the RBD. Its deletion abolished S-mediated cell membrane fusion but retained the SUreceptor-binding function indicating the possibility for a role in post-receptor binding steps of the virus entry mechanism. Interestingly, the whole soluble S ectodomain (Se) that contains the dimerization domain but not the transmembrane domain and the cytoplasmic tail forms trimers suggesting the existence of a trimerization domain in the TM subunit in its prefusion state that may lead to a conformation unfavorable for formation of higher-order multimeric structures. These results demonstrate the existence of SU dimers and Se trimers, and indicate the possibility for an unknown mechanism of their role in entry. They also further characterize the S-mediated membrane fusion and could be important for understanding the mechanisms of virus entry, and in the development of therapeutics and vaccines.
answer:
Oligomerization of the SARS-CoV S glycoprotein: dimerization of the N-terminus and trimerization of the ectodomain