In this task, you're given a paragraph and title from the research paper. Your task is to classify whether the given title is suitable or not for the research paper based on the given paragraph. Return "True" if title is proper according to paragraph else "False".

Q: Paragraph: Mannose-binding lectin (MBL) is a key soluble pathogen recognition protein of the innate immune system that binds specific mannose-containing glycans on the surfaces of microbial agents and initiates complement activation via the lectin pathway. Prior studies showed that MBL-dependent activation of the complement cascade neutralized insect cell-derived West Nile virus (WNV) in cell culture and restricted pathogenesis in mice. Here, we investigated the antiviral activity of MBL in infection by dengue virus (DENV), a related flavivirus. Using a panel of naïve sera from mouse strains deficient in different complement components, we showed that inhibition of infection by insect cell-and mammalian cell-derived DENV was primarily dependent on the lectin pathway. Human MBL also bound to DENV and neutralized infection of all four DENV serotypes through complement activation-dependent and -independent pathways. Experiments with human serum from naïve individuals with inherent variation in the levels of MBL in blood showed a direct correlation between the concentration of MBL and neutralization of DENV; samples with high levels of MBL in blood neutralized DENV more efficiently than those with lower levels. Our studies suggest that allelic variation of MBL in humans may impact complement-dependent control of DENV pathogenesis. Citation Avirutnan P, et al. 2011. Complement-mediated neutralization of dengue virus requires mannose-binding lectin. mBio 2(6):e00276-11. 
 Title: Complement-Mediated Neutralization of Dengue Virus Requires Mannose-Binding Lectin

A: True
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Q: Paragraph: This chapter seeks to survey many of the common pathological entities identified in the lungs at autopsy and the potential role of pulmonary disease in formulating an opinion regarding the cause of death. Appreciation of pulmonary pathology in the medicolegal context is important as it frequently contributes to the immediate or underlying mechanisms of death. The primacy of the lungs in breathing and their coordinated function with the cardiovascular system means that pulmonary failure can rapidly compromise tissue oxygenation and body chemistry, leading to an alteration in blood pH, hypoxic damage to downstream tissues and ultimately multiorgan failure and death. Moreover, given that the lungs have direct contact with the environment through inhalation and receive approximately 50% of the cardiac output with each beat of the heart, they may be adversely affected by hazardous agents from the outside world or other pathologic processes not primarily located in the lungs. The range of topics discussed herein is limited by design to deaths due to disease and largely foregoes discussion of more forensically relevant issues relating to toxicology or trauma. Furthermore, the content and format of this chapter is not intended to be encyclopedic, but rather attempts to highlight selected issues regarding pulmonary disease of potential relevance to surgical or forensic pathologists who perform medicolegal postmortem examinations. 
 Title: Sudden Death from Pulmonary Causes

A: False
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Q: Paragraph: The entry of enveloped viruses involves virus adsorption followed by close apposition of the viral and plasma membranes. This multistep process is initiated by specific binding interactions between glycoproteins in the viral envelope and appropriate receptors on the cell surface. In the case of HIV-1, attachment of virions to the cell surface is attributed to a high affinity interaction between envelope spike glycoproteins (Env, composed of the surface protein gp120 and the transmembrane protein gp41) and a complex made of the primary CD4 receptor and a seven-transmembrane co-receptor (e.g., CXCR4 or CCR5) (reviewed in [1]). Then a chain of dynamic events take place that enable the viral nucleocapsid to penetrate within the target cell following the destabilization of membrane microenvironment and the formation of a fusion pore. Although it is generally accepted that HIV-1 attachment to its major cellular reservoirs (i.e., T helper cells and macrophages) occurs through the twostage receptor-interaction pathway, there is accumulating evidence indicating that the initial attachment step is a more complex phenomenon than initially thought. Indeed it seems that adsorption of HIV-1 to the cell surface is modulated by a large variety of interactions between the viral entity and the target cell surface (reviewed in [2] ). This retrovirus may also attach to some cell types by CD4-independent interactions involving highly glycosylated groups or basic residues found on gp120 and polyanionic sulfated chains or lectin-like domains on some specific cell surface receptors (reviewed in [1]). For example, heparan sulfate proteoglycans, which are expressed at high levels on different cell types, such as epithelial and endothelial cells, can interact with the envelope spike glycoprotein and serve as docking structures for HIV-1 [3]. Heparan sulfate proteoglycans such as syndecans serve as the main class of attachment receptors for HIV-1 on different cell types, e.g., macrophages and endothelial cells, and are thought to play a cardinal role in virus transmission Entry Inhibitors in HIV Therapy Edited 
 Title: Attachment of human immunodeficiency virus to cells and its inhibition

A:
True
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