Detection of SARS-CoV-2 and Its Immune Response: Comparison
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Please note this is a comparison between Version 2 by Juan Carlos Hernandez Gonzalez and Version 5 by Camila Xu.

CLos coronaviruses are a large family of well- son una gran familia de patógenos bien established pathogens ofecidos de various hosts huéspedes, including domesticidos animales domésticos, animals, wildlife, andes salvajes y humanos.

  • lateral flow immunoassay
  • biosensors
  • COVID-19

1. OvDerview ofscripción general del SARS-CoV-2

CLos coronaviruses are a large family of well- son una gran familia de patógenos bien established pathogens ofecidos de various hosts huéspedes, including domesticidos animales domésticos, animals, wildlife, andes salvajes y humanos [ 1 ] . TheLos viruses that caused previous outbreaks i que causaron brotes anteriores en humanos, causing severeando enfermedades respiratory illness, lung injury, and death, areias graves, lesiones pulmonares y la muerte, son el SARS-CoV (severe acutcoronavirus del síndrome respiratory syndrome coronavirus) iio agudo severo) en 2003 and y el MERS-CoV (Middle Eastcoronavirus del síndrome respiratory syndrome coronavirus) iio de Oriente Medio) en 2012 [ 2 ] . A recent genomic analysis with severalUn análisis genómico reciente con varias herramientas bioinformatics tools showed thatáticas demostró que el SARS-CoV-2 has atiene un genome vera muy similar to the Bat al del coronavirus and theBat y el dominio de unión al receptor binding domain (RBD) of the spike glyde la glicoprotein like the Malayan pangolinína espiga como el coronavirus del pangolín malayo [ 3 ]. ThiEsta evidenceia indicates that the horseshoe bat is the natura que el murciélago de herradura es el reservoir, and the mainrio natural, y la evidence suggests that the Malayania principal sugiere que el pangolin is anín malayo es un huésped intermediate hostrio [ 3 ] .
El SARS-CoV-2 is an enveloped virus with a single-strandedes un virus envuelto con un ARN monocatenario de sentido positive-sense RNA. Theo. El tamaño del genome size of this pathogen ranges from 29.8 kb to 29.a de este patógeno varía de 29,8 kb a 29,9 kb [ 4 ] . TheEl virus encodes at leastcodifica al menos 29 proteins. The ínas. Las proteínas estructural proteins are spikees son proteínas de espiga (S), membranea (M), envelope (E), andoltura (E) y nucleocapsidápside (NP) [ 5 ] . Las proteiínas [5].no Nonestructural proteines (nsps) have functiontienen funciones necessary forarias para la replication andción y transcription in the viral lifeción en el ciclo de vida del virus cycle [ 6 ] . Viral particle size ranges from 80 to El tamaño de las partículas virales oscila entre 80 y 120 nm [ 7 ] .
TheEl mechanism of viral infection ianismo de infección viral en humans is through droplets andos es a través de gotitas y aerosols, which can travel through the aires, que pueden viajar por el aire [ 8 ] . Infection occurs in cells La infección ocurre en células que expressingan ACE2 (angiotensin-enzima converting enzyme 2) anddora de angiotensina 2) y TMPRSS2 (transmembranproteasa de serine proteasea transmembrana 2) [ 9 ] . C La proteína S del coronavirus S protein binds tose une a ACE2, the main el principal receptor del SARS-CoV-2 receptor that mediates viral entry into cells, andque media la entrada del virus en las células, y TMPRSS2 cleaves the Sescinde la protein (at the S1 and S2ína S (en las subunits) ofdades S1 y S2) del SARS-CoV-2, whichlo que facilitates the fusion of la fusión del SARS- CoV-2 and the cell y membranea celular [ 9 ] [ 10 ] [ 11 ]. In aAddition, it has been shown that the cysteineemás, se ha demostrado que las cisteína proteases cathepsin B andas catepsina B y catepsina L endosomal cathepsin L may also también pueden contribute to thisir a este processo [ 10 ] [ 12 ] [ 13 ] . In theEn el tracto respiratory tractio, ACE2 andy TMPRSS2 arse expressed in thean en las células secretory and hair cells of the nose, the seas y ciliadas de la nariz, las células secretory and hair cells of theas y ciliadas de las vías respiratorias conducting airways, in type IIoras, en las células alveolar cells in the lungs, and in the corneales de tipo II en los pulmones y en la conjunctiva of the eyetiva corneal del ojo [ 14 ] [ 15 ] [ 16 ] [ 17 ] .
The etiological virus of the pandemic has continuously evolved, with many variants emerging worldwide. Variants are categorized as the variant of interest, variant of concern, and variant under monitoring [18]. There are five SARS-CoV-2 lineages designated as the variant of concern alpha, beta, gamma, delta, and omicron variants [19]. These variants increase transmissibility compared to the original virus and potentially increase disease severity [20].

2. Immune Response against SARS-CoV-2 in Brief

The SARS-CoV-2 infection involves diverse stages in the individual: start of infection, disease development, recovery, or systemic compromise. Each infection stage triggers and modulates innate and adaptative immune system mechanisms. Although SARS-CoV-2 is a virus that humanity is learning about, the immune response is equipped with mechanisms capable of dealing with this new threat. In the initial phase of SARS-CoV-2 infection, the individual presents a presymptomatic phase lasting up to 5 days, in which a high viral load is present [21]. In these early days of infection, antibodies may not have been produced. Therefore, innate immunity is the first activated. The innate immune response comprises soluble and cellular components that respond nonspecifically against the virus. The cellular compounds include dendritic cells (DC), monocytes, macrophages, neutrophils, natural killer (NK) cells, and other innate lymphoid cells (ILCs) [22]. Whereas soluble components include complement systems, soluble proteins, interferons, chemokines, and naturally occurring antibodies [23]. Immune response cells recognize pathogen-associated molecular patterns (PAMPs) of SARS-CoV-2 through pattern recognition receptors (PRRs) such as Toll-like receptors (TLR), RIG-I-like receptors (RLR), and melanoma differentiation-associated protein 5 (MDA5). The viral sensing triggers the activation of signaling pathways which induce the production of immune mediators to generate an antiviral state mainly mediated by type I (IFN-α/β) and type III (IFN-λ) interferons (IFNs) [24]. Reports have described that robust IFNs production during the early stage of infection is required to have a protective innate immune response against the virus [25]. On the contrary, an inadequate and slow response to type I and type III IFNs due to virus evasion mechanisms, host comorbidities, or genetic defects cause an exacerbated immune response. This inadequate response induces elevated levels of chemokines (CCL2, CCL8, CXCL2, CXCL8, CXCL9, and CXCL16), high expression of proinflammatory cytokines such as IL-6, IL-10, IL-1, and TNF, in addition to activation, and recruitment of immune cells [26][27]. The called “cytokine storm” leads to unbalanced levels of proinflammatory and antiviral mediators that remain the leading cause of ARDS and multi-organ failure [25][26][28].
On the other hand, the adaptive immune response is orchestrated by CD8+ T lymphocytes, TCD4+, and B lymphocytes, responsible for immunological memory. In response to SARS-CoV-2 infection, it has been shown that non-severe patients or patients with mild symptoms have a low viral load and may not have produced antibodies [29][30]. In contrast, antibodies have been detected by immunoassay tests and biosensors in patients with severe symptoms or cases [29][31]. Patients with a high viral load activate the humoral immune response in the first two weeks of infection [32]. The first seroconversion of antibodies is against protein N, followed by protein S of SARS-CoV-2 in patients with disease symptoms [33]. Immunoglobulins IgA and IgM begin to be detected within the first ten days of infection; however, both antibodies can cross-react with protein N, which is highly conserved among coronaviruses [34][35]. Moreover, high levels of IgG1 and IgG3 are expressed ten to fourteen days after infection in patients with disease symptoms [36][37]. Older adults and seriously ill individuals reach high specificity antibodies concentrations against SARS-CoV-2 S protein.
Due to the urgency of reducing thousands of people’s cases and deaths, scientists have developed several vaccines against COVID-19. Efforts are being made to apply vaccines with emergency use authorization to the world population. Vaccination elicits immune responses capable of potently neutralizing SARS-CoV-2. However, the available data show that most approved COVID-19 vaccines protect against severe disease but do not prevent the clinical manifestation of COVID-19 [38]. Instead, it has been demonstrated that new variants with mutations in the spike, the main target of neutralizing antibodies, can escape the neutralization of humoral immunity [39][40].

3. SARS-CoV-2 Detection

Molecular tests or biosensors are the tools for detecting SARS-CoV-2 nucleic acids/ antigens/antibodies against the virus (Figure 1). In the early part of the illness, viral particles and their subunits can be detected; beyond the first two weeks of illness onset, antibodies against the virus could be detected [41]. The SARS-CoV-2 infection stage is highly correlated to the diagnostic technique recommended for the pandemic. Early diagnosis of the disease and isolation of infected people is key to controlling the transmission of SARS-CoV-2 [42][43]. In the initial phase of SARS-CoV-2 infection, the individual presents a presymptomatic phase lasting up to 5 days, in which a high viral load is present [21]. During these early days of infection, antibodies may not be detected. Therefore, since the pandemic began, the diagnostic method has been based on detecting viral genes using the molecular PCR technique, the gold standard worldwide [44][45][46]. The pandemic has exceeded the ability to identify the virus in laboratories using molecular techniques; this has motivated the development of new technologies for the rapid detection of SARS-CoV-2 that are easy to perform compared to molecular tests in clinical laboratories. LFIA has been the unique device approved and available to use in mass worldwide. Biosensors with transducers are developing in SARS-CoV-2 diagnostic. However, most nanomaterials used in these biosensors present interferences with contaminants in human samples compared to performance under experimental conditions. It is important to emphasize that LFIAs have the unique properties of availability, accessibility, economy, and POC (including home use), these characteristics that are not shared by all biosensors with a transducer. In addition, biosensors with transducers require exclusive handling in laboratories certified under the Clinical Laboratory Improvement Amendments of 1998 [47][48]. The FDA have to date approved only one piezoelectric biosensor [47] (Figure 1).
Biosensores 12 00728 g001 550
Figure 1.  Principle of LFIA test.io de la prueba LFIA. La prueba LFIA test detects the target molecule on ana la molécula objetivo en una membrana absorbent membrane with antibodies aligned to form the test ande con anticuerpos alineados para formar las líneas de prueba y control lines. The sample is placed on a sample pad, then migrates to th. La muestra se coloca en una almohadilla de muestra, luego migra a la almohadilla de conjugate pad, which contains the immobilized conjugate, usually made of do, que contiene el conjugado inmovilizado, generalmente hecho de nanoparticles (colículas (oro coloidal gold,, látex colored orado o fluorescent latex,e, celulosa colored celluloseada) conjugated to antibodies or antigens. The sampledas con anticuerpos o antígenos. La muestra interacts with theúa con el conjugate, and bothdo y ambos migrate to the next section of the strip, where the biologicaln a la siguiente sección de la tira, donde se inmovilizan los components of the assayes biológicos del ensayo (proteinínas/antibodies/antigens) are immobilized. In this section, the analyte and cuerpos/antígenos). En esta sección, se capturan el analito y el conjugate are captured. Excess reagent passes through thado. El exceso de reactivo pasa a través de las líneas de capture lines and accumulates on thea y se acumula en la almohadilla absorbent pad. Thee. Los results arados se interpreted on than en la membrana de nitrocellulose membrane as the ulosa como la presence or absence of the test andia o ausencia de las líneas de prueba y control lines.

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