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: 2 The abbreviations used are: S, spike; SARS-CoV, severe acute respiratory syndrome coronavirus; MLV, murine leukemia virus; DC-SIGN, dendritic cell-specific intercellular adhesion molecule-3-gubbing non-integrin, ACE2, argiotensin I conserting enzyme 2. FIGURE 4. Introduction of alanine residues in the S2 region modulates elastase-induced virus entry mediated by SARS-CoV S. A and B, pseudotyped virion infections were performed as described for Fig. 2. Infection was induced by treatment with elastase (A) or trypsin (B). Results are presented as relative light units (RLU). Error bars represent the S.E. of three independent experiments. C, cleavage of SARS-CoV by elastase. HEK293T cells expressing the wild type (WT) or mutant SARS-CoV spike protein were treated with 50 g/ml elastase. Cell surface proteins were biotinylated and precipitated, and cleavage products of the SARS-CoV spike protein were analyzed in Western blot with an antibody recognizing the C9 tag at the C terminus of the protein.

A: Elastase-mediated Activation of the Severe Acute Respiratory Syndrome Coronavirus Spike Protein at Discrete Sites within the S2 Domain * S
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Q: A novel coronavirus, termed the severe acute respiratory syndrome coronavirus (SARS-CoV), infected humans in Guangdong, China, in November 2002 and the subsequent efficient human-to-human transmissions of this virus caused profound disturbances in over 30 countries worldwide in 2003. Eventually, this epidemic was controlled by isolation and there has been no human infection reported since January 2004. However, research on different aspects of the SARS-CoV is not waning, as it is not known if this virus will re-emerge, especially since its origins and potential reservoir(s) are unresolved. The SARS-CoV genome is nearly 30 kb in length and contains 14 potential open reading frames (ORFs). Some of these ORFs encode for genes that are homologous to proteins found in all known coronaviruses, namely the replicase genes (ORFs 1a and 1b) and the four structural proteins: nucleocapsid, spike, membrane and envelope, and these proteins are expected to be essential for the replication of the virus. The remaining eight ORFs encodes for accessory proteins, varying in length from 39 to 274 amino acids, which are unique to SARS-CoV. This review will summarize the expeditious research on these accessory viral proteins in three major areas: (i) the detection of antibodies against accessory proteins in the serum of infected patients, (ii) the expression, processing and cellular localization of the accessory proteins, and (iii) the effects of the accessory proteins on cellular functions. These in-depth molecular and biochemical characterizations of the SARS-CoV accessory proteins, which have no homologues in other coronaviruses, may offer clues as to why the SARS-CoV causes such a severe and rapid attack in humans, while other coronaviruses that infect humans seem to be more forgiving.

A: Understanding the accessory viral proteins unique to the severe acute respiratory syndrome (SARS) coronavirus
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Q: Three tests were compared to diagnose herpes virus infection: electron microscopy (EM), viral culture (VC) and cytodiagnosis (Tzanck smear). The study comprised 67 patients with skin or mucous membrane lesions suggestive of herpes simplex virus (HSV) infection. The sensitivity of EM increased 25% after virus concentration by ultracentrifugation. Herpes virus infection was confirmed in 55 of the 67 cases by EM or VC or both. EM detected 53 herpes virus-positive lesion samples of which 14 were not detected by VC; only two lesion samples that were herpes virus-positive in VC were not detected by EM. The sensitivities of EM, VC, and Tzanck smear for the group of 55 herpes virus-positive cases were 96%, 75% and 76%, respectively. The specificity of the Tzanck smear was 83% (prevalence 82%). Colloidal gold immuno-EM was used to rapidly type HSV-1, HSV-2 and varicella zoster virus (VZV) present in skin and mucous membrane lesions in less than 4 h. Immuno-EM was able to detect antiviral antibodies on viral envelopes and viral cores in lesion samples with negative VC. Antiviral antibodies do not interfere with typing of herpes viruses by immuno-EM. It is suggested that formation of viral immune complexes and inactivation of virus particles by antibodies may have caused a Correspondence to: E. Folkers,

A:
Improved detection of HSV by electron microscopy in clinical specimens using ultracentrifugation and cdlloidal gold immunoelectron microscopy: comparison with viral culture atld, cytodiagnosis
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