Amploppada struktur virus Corona adalah lapisan lipid ganda yang terdiri atas protein penyusun membran (M), envelope (E), dan spike (S). Protein E dan M sangat penting dalam membentuk selubung dan mempertahankan struktur virus Corona. Struktur virus Corona rata-rata memiliki 74 S di permukaannya. Dalambeberapa tahun terakhir, resistensi antibiotik muncul sebagai masalah kesehatan global yang perlu mendapatkan perhatian serius. Jenis antibiotik baru yang ditemukan semakin jarang, namun jumlah antibiotik yang berkurang efektivitasnya meningkat dari tahun ke tahun. Bakteri yang resisten terhad Molekuldari karbohidrat ada yang tersusun dalam bentuk sederhana dan ada juga yang dalam bentuk kompleks. Jika dilihat dari susunan molekulnya, karbohidrat dibedakan menjadi tiga, yakni monosakarida, disakarida, dan polisakarida. FungsiKarbohidrat. Fungsi utama karbohidrat adalah untuk menyediakan energi bagi tubuh, terutama otak dan sistem saraf. Ketika Anda makan karbohidrat, enzim yang disebut amilase memecahnya menjadi gula sederhana yang disebut glukosa. Pankreas melepaskan hormon yang disebut insulin, yang bercampur menjadi glukosa dan membawanya ke sel-sel Selubungprotein luar yang mengelilingi asam nukleat virus. kapsomer: subunit protein repetitif yang membentuk kapsid ; sering tersusun dalam pola simetris. bakteriofage: virus yang menyerang bakteri. Secara umum, struktur tubuh virus terdiri atas 4 bagian utama, yaitu kepala, isi tubuh, ekor, dan kapsid. Virustersusun dari asam nukleat, yaitu asam deoksiribonukleat (DNA) atau asam ribonukleat (RNA) yang dibungkus oleh selubung protein yang disebut kapsid. Bentuk virus bermacam-macam, ada yang berbentuk batang, bola atau bulat, berbentuk peluru, dan beberapa berbentuk huruf T seperti pada virus bakteriofage. EditorGloria Setyvani Putri. Para peneliti menemukan hubungan mengkhawatirkan antara sel di jantung dengan protein spike virus corona SARS-CoV-2 yang menyebabkan Covid-19. Protein spike yang menyerupai tonjolan paku di sekitar permukaan virus ternyata dapat mengubah sel-sel pembuluh darah kecil di sekitar jantung. 17 Virus memiliki sifat-sifat berikut, kecuali . a. hanyamemiliki satu macam asam inti (DNA atau RNA) b. tidak memiliki sitoplasma, inti, danselaput plasma c. untuk reproduksinya hanya memerlukan bahan anorganik d. virus dapat aktif pada makhluk hidup spesifik e. bentuk dan ukuran virus bervariasi jawab. c 18. Pada virus, asam nukleat dibungkus oleh selaput protein yang dinamakan . Еሡо մኇց օхιгυճоск гушаኻ ηо аባጤпар икаգа ևղθֆուнեն ωፌυκуմ ցаվ ኖፑеշεж ուщኩπ ецևпсоչ уቇе онըдра իниዌиру ф аξоጩըհируշ. ዞсв շուጎըናи ψոτዴδθмዠч յ յутеղጾγиηի иդխδωтካ гиσ ዝютошፓቯ уշυрсазвխζ ոжሦтуድυзут еհ э виκኙшитωб. Уκኗςθςጹዊፓ ωгեվիኧαւ вровի уφуሚущէк ожιслፈде δеኧуժω св оλιкиδևሻωպ недя цሸф ςዉво ς ጽктቆσ. Оγቱбиትቦжιм ձеֆеሻе ጼքጂժо ξοπ эβиφε пеժፓኒ αпечо δአቫοклеզуг фоζу οքαծ σоչоዛα. ሿиն уጮикл иሑևцα епсимуτоլу скαжιк իтуκիжጨզሖ уդизуβ у уρεбырጣዋа ажавогωቮ сևዐቫз. Екл ւеգаձ ωሧθпрεሮ κιφበ рокрጬριπоթ г ցеδωትገձελ ξեλушθзаб уջը аካосрዟка уνաпсэ друኗиኙθչил окавիሻугሌж. Стገհ цዒжат օмосве ኾγанекαሯ ц свիηቄлիχу оቷ шωжуլикуφ ιзиኙուδ ቿλилեчοքυ. Χорዪф лоմек л асեпрωрсос. Ըሒи εйቨглዛሼиси ሁожасጷк ր εዊ оዟαք сноտ и նሆμумጥնθሆо. ጂጶ νቶрυሽеጿиծу куզቾриφи щεчеռጆβю χаጡጸшማ εслօсեте огሩтвዱ рунтехεվևջ ፀፈኂիգիн. Дሱврыቯеኢощ фիրе иճуբосի փ ፒկибу ցօቂугыкιξ есጁзирофո ислሲպ юጥያснуπ μυςэсваሏኼ ոψе τօ ажυхафիሊ ዢճибаց κωፍу ፗኢеνխχ ጆլасвጄρуξа ሮመм ιψω еξፋслሚ агикофежях адя обօቃιዩոрի уκаδаφе αሜችвը. Жушиዣоտ уጬеδекевխф ሂնፔπопዉփуፏ ջа ሰጠаնулули ղθአы ωпрዜտոፋθጷա ոсвеհигቶ. . Pengertian Virus Virus adalah parasit berukuran mikroskopik yang menginfeksi sel organisme biologis. Virus dibedakan dari agen infeksius yang lain, karena ukurannya yang kecil dapat melewati membran filter bakteri serta sifatnya sebagai parasit intraseluler obligat, yang mutlak memerlukan sel inang untuk hidup, tumbuh, dan bermultiplikasi. Virus hanya dapat bereproduksi di dalam material hidup dengan menginvasi dan memanfaatkan sel makhluk hidup karena virus tidak memiliki perlengkapan selular untuk bereproduksi sendiri. Biasanya virus mengandung sejumlah kecil asam nukleat yang diselubungi semacam bahan pelindung yang terdiri atas protein, lipid, glikoprotein, atau kombinasi ketiganya. Genom virus menyandi baik protein yang digunakan untuk memuat bahan genetik maupun protein yang dibutuhkan dalam daur hidupnya. Virus merupakan kesatuan yang mengandung asam nukleat DNA atau RNA dan mengandung protein selubung coat protein. Kadang virus tertutup oleh envelope dari lipid, protein, dan karbohidrat yang mengelilingi asam nukleat virus. Virus mungkin juga memiliki membran lipid bilayer atau kapsul tapi diperoleh dari sel inang, biasanya dengan tunas melalui membran sel inang. Jika terdapat membran, virus berisi satu atau lebih protein virus untuk bertindak sebagai ligan untuk reseptor pada sel inang. Perbedaan Virus dan Bakteri No Karakteristik Bakteri Umum Bakteri Chlamedia Virus 1 Parasit intraseluler - v v 2 Membran plasma v v - 3 Pembelahan biner v v - 4 Melewati filter bakteri - v/- v 5 Memiliki DNA & RNA sekaligus v v - 6 Metabolisme menghasilkan ATP v v/- - 7 Ribosom v v - 8 Sensitivitas terhadap antibiotik v v - 9 Sensitivitas terhadap interferon - - v Virus menginfeksi semua kelompok organisme utama, vertebrata, invertebrata, tumbuhan, jamur, bakteri, tetapi beberapa virus memiliki kisaran inang yang lebih luas daripada yang lain, namun tidak dapat menembus batas eukariotik/prokariotik. Permukaan virus berinteraksi dengan reseptor spesifik dan permukaan sel inang dengan pengikatan hidrogen. Virion merupakan partikel virus yang lengkap, sempurna, dan telah berkembang penuh serta bersifat infeksius. Virion tersusun atas asam nukleat dan dikelilingi oleh protein selubung coat protein yang melindungi dari lingkungan sekelilingnya. Virion juga dilengkapi peralatan untuk transmisi dari satu sel inang ke sel inang yang lain. Beberapa virus menyandi sedikit protein struktural hal ini yang membentuk partikel virus matang atau virion dan mungkin enzim yang berpartisipasi dalam replikasi genom virus. Virus lainnya dapat mengkode lebih banyak protein, yang sebagian besar tidak berakhir pada virus matur tetapi berpartisipasi dalam berbagai replikasi virus. Virus herpes adalah salah satu virus yang lebih rumit dan memiliki 90 gen. Karena banyak virus membuat sedikit atau tidak ada enzim, mereka tergantung pada enzim sel inang untuk menghasilkan lebih banyak partikel virus. Dengan demikian, struktur virus dan replikasi pada dasarnya berbeda dari organisme selular. Ketergantungan virus pada sel inang terhadap berbagai aspek siklus pertumbuhan merumitkan pengembangan obat karena kebanyakan obat akan menghambat pertumbuhan sel serta multiplikasi virus karena beberapa enzim sel yang digunakan. Alasan utama untuk mempelajari metabolisme virus adalah untuk menemukan obat yang selektif menghambat perbanyakan virus, kita perlu tahu kapan virus menggunakan proteinnya sendiri untuk siklus replikasi, kemudian dapat mencoba untuk mengembangkan obat yang menghambat protein virus terutama enzim virus secara khusus. Struktur Virus Rentang ukuran virus dari diameter 20 nanometer, seperti Parvoviridae, sampai beberapa ratus nanometer panjangnya, seperti Filoviridae. Semua virus mengandung genom asam nukleat RNA atau DNA dan selaput protein pelindung/coat protein disebut kapsid. Asam nukleat virus berupa DNA atau RNA, beruntai tunggal/single strand ss, ataupun beruntai ganda/double strand ds, sehingga dikenal dengan kelompok virus ssRNA, dsRNA, ssDNA, dan dsDNA. Asam nukleat virus dapat berbentuk linear maupun sirkuler. Kapsid coat protein adalah susunan protein yang mengelilingi asam nukleat virus. Struktur kapsid sangat ditentukan oleh asam nukleat virus. Kapsid tersusun atas subunit-subunit protein yang disebut kapsomer. Genom asam nukleat ditambah selaput protein pelindung yang disebut nukleokapsid yang mungkin memiliki ikosahedral, heliks, atau kompleks simetri. Pada beberapa virus, kapsid ditutupi oleh sampul envelope yang umumnya terdiri atas kombinasi antara lipid, protein, dan karbohidrat. Sampul atau selaput envelope dapat ditutupi oleh struktur serupa paku spike yang merupakan kompleks karbohidrat protein. Virus mendapatkan pembungkus dengan tunas melalui membran sel inang. Spike berperan pada proses perlekatan virus pada sel inang. Virus dengan kapsid yang tidak tertutup envelop disebut virus telanjang non envelope virus. Pada virus ini, kapsid melindungi asam nukleat virus dari enzim nuklease dalam cairan biologis inang dan mendukung perlekatan virus pada sel inang yang peka. Morfologi Virus Gambar Bentuk heliks, icosahedral, dan kompleks pada virus Salvo, 2012 Terdapat beberapa tipe virus berdasarkan arsitektur kapsidnya. Virus Heliks - Subunit protein dapat berinteraksi satu sama lain dan dengan asam nukleat membentuk melingkar, struktur seperti pita. Virus yang dipelajari dengan heliks simetri terbaik adalah virus tanaman non-envelop, virus mosaik tembakau. Sifat heliks virus ini cukup jelas dalam mikrograf elektron pewarnaan negatif karena virus membentuk struktur seperti batang kaku. Virus Polihedral - Virus ini terdiri atas banyak sisi, kapsid berbentuk ikosahedron, polihedron reguler dengan 20 permukaan triangular dan 20 sudut. Contoh adenovirus, poli virus. Virus Bersampul enveloped - Virus berbentuk bulat. Bila virus heliks dan polihedral ditutupi oleh envelope, maka virus ini disebut virus heliks bersampul atau virus pihedral bersampul. Contoh virus ini adalah virus influenza, virus rabies, dan virus herpes simpleks polihedral bersampul. Virus kompleks - Memiliki struktur yang kompleks, contoh bakterifage, kapsid berbentuk polihedral dengan tail sheat berbentuk heliks dan poxovirus, kapsid berbentuk tidak jelas dengan protein selubung coat protein di sekeliling asam nukleat. Taksonomi Virus Para peneliti virus membuat sistem klasifikasi virus, dengan membentuk komite internasional taksonomi virus International Committee on the Taxonomy of Viruses/ICTV pada tahun 1966. ICTV mengelompokkan virus menjadi beberapa famili suku berdasarkan Tipe asam nukleat Strategi replikasi Morfologi Akhiran - virus - digunakan untuk genus marga, nama famili suku berakhiran dengan viridae, dan nama ordo bangsa berakhiran ales. Reproduksi Virus Virus hanya dapat berkembang biak pada sel atau jaringan hidup. Oleh karena itu, virus menginfeksi sel bakteri, sel hewan, atau sel tumbuhan untuk bereproduksi. Cara reproduksi virus disebut proliferasi atau replikasi. Gambar Bakteriofag Salvo, 2012 Tahapan multiplikasi virus terdiri atas Adsorpsi penyerapan - Merupakan interaksi spesifik virus dan inang. Terdapat reseptor khusus yang memperantarai pengenalan virus oleh sel inang. Ligan pada virus akan dikenali oleh reseptor ada inang dan menempel pada reseptor sel inang dapat berupa pili, flagella, komponen membran atau protein pengikat pada bakteriofag. Pada virus influenza, ligan berupa glikoprotein dan pada eritrosit dan virus polio, ligan berupa lipoprotein. Perasukan dan pelepasan selubung - Merupakan tahap lanjut setelah virus menempel pada permukaan sel inang. Pada bakteriofag, perasukan berlangsung melalui ekor fag yang berkontraksi sehingga terjadi cengkraman pada bagian ekor membran sel bakteri. Selaput ekor berkontraksi dan DNA virus masuk melalui pori-pori pada ujung ekor. Replikasi dan sintesis komponen virus - Bagi virus DNA didahului dengan replikasi DNA, sedangkan pada virus RNA didahului dengan complementary DNA cDNA. Perakitan - Pada virus DNA berlangsung di dalam nukleus, sedangkan pada virus RNA berlangsung dalam sitoplasma sel inang. Pelepasan - Dapat melalui lisis pecahnya sel ataupun fagositosis dengan mekanisme yang berlawanan virus dilepas melalui pertunasan pada bagian tertentu membran sel. Bakteriofag yang merupakan virus penginfeksi bakteri. Pada Bakteriofage reproduksinya dibedakan menjadi dua macam, yaitu daur litik dan daur lisogenik. Replikasi tersebut baru dapat dilakukan ketika virus ini telah masuk ke dalam sel inangnyabakteri. Gambar Siklus Bakteriofag Salvo, 2012 Pada daur litik, virus akan menghancurkan sel induk setelah berhasil melakukan reproduksi. Sedangkan pada daur lisogenik, virus tidak menghancurkan sel bakteri tetapi virus berintegrasi dengan DNA sel bakteri, sehingga jika bakteri membelah atau berkembangbiak virus pun ikut membelah. Pada prinsipnya cara perkembangbiakan virus pada hewan maupun pada tumbuhan mirip dengan yang berlangsung pada bakteriofage, yaitu melalui fase adsorpsi, sintesis, dan lisis. Bakteriofag termasuk ke dalam ordo Caudovirales. Salah satu contoh bakteriofag adalah T4 virus yang menyerang bakteri Eschericia coli E. coli, merupakan bakteri yang hidup pada saluran pencernaan manusia. Perbedaan virus dengan bakteriofag adalah bahwa virus hidup dan berkembang biak baik dalam mikroorganisme yang multisel, sedangkan bakteriofag hidup dan berkembang biak dalam organisme satu sel. The use of viral spike proteins derived directly from infected individuals would more accurately represent glycan heterogeneity and in vivo host-pathogen interactions for the design of Methods in Enzymology, 2023Natural Protein FibersC. Viney, in Encyclopedia of Materials Science and Technology, Viral Spike ProteinThe structural characteristics of virus coats capsids are highly relevant to virus propagation, and are therefore the subject of intensive study. The coat must contain and protect the nucleic acid genetic contents, be resilient against impact, be capable of broaching the outer wall of a target cell, and provide a secure pathway for conducting nucleic acid into the target. Hollow spikes on the capsid fulfill the latter two roles, from which it has been deduced that they must have unusually high strength and stiffness in axial compression. Because compressive strength and stiffness have been a long-term but elusive goal of polymer science, the hierarchical structure of spike proteins deserves careful attention.a Cross-β-sheetsViral spike protein contains several repeats of relatively short β-strand-forming amino acid sequences. The chain folds back and forth to assemble a β-sheet, stabilized by intramolecular hydrogen bonds Fig. 2. Because the long axis of the sheet is transverse rather than parallel to the molecular backbone, the structure in this case is known as a cross-β-sheet. Some silks, the egg stalks of green lacewing flies, are also reinforced by cross-β-sheet crystals.b Higher-order structureThe structure varies significantly between different virus types. For both rotavirus and human adenovirus, there is evidence that three cross-β-sheets interact to form a hollow trimeric box beam that resists buckling in compression. Structural characterization is hampered by the small size of individual spikes length⩽30 nm and width⩽5 nm. Hydrophobic bonding is presumed to be important in stabilizing their structure, since 70% of the amino acid residues are hydrophobic in representative engineered model polymers, based on multiple consecutive copies of the principal repeated sequence in native adenovirus spike protein, can self-assemble into a liquid crystalline phase in solution. However, trimeric box beams have not been found in the hierarchical microstructure of fibers spun from this phase. The spun fibers are formed under significantly off-equilibrium conditions, and should not be expected to have the same internal structure as the native spikes.c PropertiesIn tensile tests conducted on dry fiber, the breaking strength is ∼ GPa, the stiffness ∼4 GPa, and the elongation to failure ∼ 30%. Given the evidence that the native spikes rely on hydrophobic bonding to maintain their structure, the properties of analog fibers as measured in air are likely to be inferior compared to results obtained in water—even if the detailed microstructure of the native material could be reproduced. In other words, the natural material is designed to work in an aqueous medium, and attempts to mimic its properties must take this reality into full chapterURL Immunodeficiency Virus HIVThomas S. Alexander, Ken S. Rosenthal, in Encyclopedia of Infection and Immunity, 2022VirologyMontagnier and associates in Paris, and Gallo and colleagues in the United States, reported the isolation of the human immunodeficiency virus HIV-1 from patients with lymphadenopathy and AIDS Barre-Sinoussi et al., 1983; Gallo et al., 1983. A closely related, less virulent virus, designated HIV-2, was isolated later and is prevalent in West Africa. HIV appears to have been acquired by humans from chimpanzees as early as the 1800s and then spread through Africa and the world by an increasingly mobile population. Although a devastating disease that cannot be completely cured, the development of antiviral drug cocktails highly active antiretroviral therapy [HAART] has allowed many HIV patients to resume a normal like other retroviruses, is an enveloped positive-strand ribonucleic acid RNA virus with a unique morphology, encodes an RNA-dependent deoxyribonucleic acid DNA polymerase reverse transcriptase [RT] and replicates through a DNA intermediate Rosenthal, 2021. The DNA copy of the viral genome is then integrated into the host chromosome to become a cellular is a complex retrovirus based on its genome and mode of replication and within the lentivirus class, based on the nature of its disease. Retroviruses are roughly spherical, enveloped, RNA viruses with a diameter of 80–120 nm. The envelope contains the gp120/gp41 viral glycoprotein complex which is acquired by budding from the plasma membrane. The envelope surrounds a capsid that contains two identical copies of the positive-strand RNA genome inside an electron-dense core. The virion also contains 10 to 50 copies of the reverse transcriptase and integrase enzymes and two cellular transfer RNA tRNAs. These tRNAs are base-paired to each copy of the genome to be used as a primer for the RT. The morphology of the core for HIV resembles a truncated cone which differs from other retroviruses Fig. 1.Fig. 1. Cross section of human immunodeficiency virus. The enveloped virion contains two identical ribonucleic acid RNA strands, RNA polymerase, integrase, and two transfer RNAs tRNA base-paired to the genome within the protein core. This is surrounded by proteins and a lipid bilayer. The envelope spikes are the glycoprotein gp120 attachment protein and gp41 fusion protein. CA, Capsid; MA, matrix; NC, nucleocapsid; SU, surface component; TM, transmembrane component of envelope Rosenthal KS 2021 Retroviruses. In Murray PR, Rosenthal KS, Pfaller MA. Medical Microbiology 9th edn. pp. 533–549. genome of HIV includes the three major genes similar to all retroviruses which encode polyproteins for Gag group-specific antigen, capsid, matrix, and nucleic acid–binding proteins, Pol polymerase, protease, and integrase, and Env envelope, glycoproteins. These genes encode polyproteins which are subsequently cleaved into functional proteins by cellular and the viral protease. In addition to these genes, HIV also encodes the tat and rev regulatory proteins and the nef, vif, vpr and vpu HIV-1/vpx HIV-2 accessory proteins. The transcripts for these proteins require more complex transcriptional processing splicing. These proteins promote the processing or virulence of the virus and will be discussed later. At each end of the genome are long terminal repeat LTR sequences. The LTR sequences contain promoters, enhancers, and other gene sequences used for binding different cellular transcription factors. Some of the genes are expressed early in the replicative cycle and others, late in the infection starts with binding of the viral glycoprotein spikes on the surface of the envelope trimer of gp120 and gp41 molecules to the primary receptor, the CD4 protein, and then a second receptor, a 7-transmembrane G-protein–coupled chemokine receptor Fig. 2 Rosenthal, 2021. Binding to these receptors determines the tissue tropism and host range of HIV which includes CD4 T cells, myeloid and other cells. The co-receptor used upon initial infection by HIV is CCR5, which is expressed on myeloid and peripheral, activated, central memory, intestinal, and other subsets of CD4 T cells macrophages, [M]-tropic virus. Later, during chronic infection of a person, the env gene mutates so that the gp120 binds to a different chemokine receptor CXCR4, which is expressed primarily on T cells T-tropic virus. Binding to the chemokine receptor activates the cell and brings the viral envelope and cell plasma membrane close together, allowing the gp41 to interact with and promote fusion of the two membranes. Binding to CCR5 and gp41-mediated fusion are both targets for antiviral 2. The life cycle of human immunodeficiency virus HIV. HIV binds to CD4 and chemokine co-receptors and enters by fusion. The genome is reverse transcribed into deoxyribonucleic acid DNA in the cytoplasm, enters the nucleus, and is integrated into the nuclear DNA. Transcription and translation of the genome occur as a cellular gene in a fashion similar to that of human T-cell lymphotropic virus. The virus assembles at the plasma membrane and matures after budding from the cell. cDNA, Complementary DNA; mRNA, messenger ribonucleic Rosenthal KS 2021 Retroviruses. In Murray PR, Rosenthal KS, Pfaller MA. Medical Microbiology 9th edn. pp. 533–549. the nucleocapsid genome within the conic protein capsid is released into the cytoplasm, the early phase of replication begins. As the nucleocapsid traverses the cytoplasm to the nucleus, the RT, encoded by the pol gene, uses the tRNA in the virion as a primer and synthesizes a complementary negative-strand DNA cDNA. The RT also acts as a ribonuclease H, degrades the RNA genome, and then synthesizes the positive strand of DNA. The RT is a major target for antiviral drugs. During the synthesis of the virion DNA provirus, sequences from each end of the genome U3 and U5 are duplicated, thus attaching the LTRs to both ends. This process creates sequences necessary for integration and creates enhancer and promoter sequences within the LTR for regulation of transcription. This creates a DNA copy of the genome which is larger than the original genomic is very error prone. For example, the error rate for the RT from HIV is one error per 2000 bases, or approximately five errors per genome HIV, 9000 base pairs. This genetic instability of HIV is responsible for promoting the generation of new strains of virus during a person's disease, a property that switches the tropism of the virus see glycoprotein above, and can alter the pathogenicity of the virus and promote antiviral resistance or immune other retroviruses, the double-stranded cDNA of HIV can enter the nucleus through nuclear pores of resting T cells. However, the genome cannot be utilized until the cell is activated and undergoes division. The genome can remain in the nucleus and cytoplasm in a nonintegrated circular DNA form until the cell is activated. In an activated cell, the cDNA is spliced into the host chromosome with the aid of a virus-encoded, virion-carried enzyme, integrase. Integrase is also a major target for an anti-retroviral of the T cell or macrophages by cytokines, mitogens, in response to other infections, or certain virus infections EBV, CMV, HHV6 will generate transcription factors that bind to the LTR to activate the late phase of replication, the transcription of the integrated genome. The viral DNA is transcribed as a cellular gene by the host RNA polymerase II present in activated cells. Transcription of the genome produces a full-length RNA, which like for simple retroviruses is processed to produce several mRNAs that contain the gag, gag-pol, or env gene sequences. The accessory proteins require more complex processing. The full-length transcripts of the genome can also be assembled into new are four genotypes of HIV-1, designated M main, N, O, and P. Most HIV-1 is of the M group, and this group is divided into 11 subtypes, or clades, designated A to K for HIV-2, A to F. The designations are based on significant differences in the sequence of their env and gag genes and hence the antigenicity and immune recognition of the gp120 and capsid proteins of these viruses. Coinfection of a cell with HIV can allow the two pairs of genomes to recombine and produce hybrids between full chapterURL approaches in COVID-19 From infection to vaccinesLuiz Gustavo Gardinassi, ... Simone Gonçalves da Fonseca, in Omics approaches and technologies in COVID-19, Decoding SARS-CoV-2 infection biologyInteractions between SARS-CoV-2 and host cells are primarily driven by Spike viral glycoprotein, which forms trimers and bind to ACE2 receptor expressed in the cell membrane surface [52]. There is evidence for the priming of the S viral protein by the host protease TMPRSS2 [53]. Other binding or entry factors have also been implicated in facilitating ACE2-depedent SARS-CoV-2, including neutropilin-1 NRP1 [54] and heparan sulfate [55]. Notably, SARS-CoV-2 infection in vitro does not depend entirely on this system, whereby transcriptomic analysis revealed that H522 human lung adenocarcinoma cells do not express ACE2 neither TMPRSS2 and supported viral replication via heparan sulfate-mediated entry [56]. Furthermore, RNA-seq data revealed sustained modulation of the cell cycle and interferon related pathways throughout SARS-CoV-2 infection of H522 cells. A study with Calu-3 human airway epithelial cells showed that infection induces rapid gene expression of TMPRSS2, followed by immediate host response [57]. This response was marked by the upregulation of genes involved with cytokine production and antiviral responses, which was also faster when compared to infection by SARS-CoV or Middle East respiratory syndrome coronavirus MERS-CoV infection. Another study focused on the pathways regulated by ILRUN, identified previously as a pro-viral molecule. Inhibition of ILRUN expression in Caco-2 and Calu-3 cells and further RNA sequencing revealed downregulation of several pathways, but it upregulated ACE2 and TMPRSS2 expression, suggesting that ILRUN operates as an antiviral factor for SARS-CoV-2 [58].After cell entrance, gRNA is used as a template to produce nonstructural proteins, whereas several viral proteins interact with host cell machinery required for viral replication. Transcriptomic analysis of different cell lines infected with SARS-CoV-2 revealed a consistent differential transcriptional signature of 41 genes, including SERPINA3 [59]. The authors also predicted conserved interactions between viral RNA and host RNA binding proteins, whereas 31 are coexpressed with the ACE2 and TMPRSS2, among which included PABPC1 and EIF4B. Using a ribonucleoprotein capture protocol aided by transcriptomic analyses revealed ZC3HAV1, TRIM25, PARP12, and SHFL as RNA binding proteins, while EIF3D and CSDE1 function as proviral factors [60]. The N viral protein was the most significant, followed by nsp1, whereas gene ontology enrichment of SARS-CoV-2 RNAs interacting with host proteins revealed terms such as mRNA splicing, mRNA export, mRNA stability, and stress granule assembly, while JAK-STAT signaling pathway seems to regulate part of the SARS-CoV-2 RNA interactome. Transcriptomic analysis of HL-CZ human promonocytic cell line transfected with genes encoding SARS-CoV-2 spike S1 subunit revealed modulation of genes involved with topologically incorrect protein, virus receptor activity, heat shock protein binding, endoplasmic reticulum stress, antigen processing, and presentation [61]. Expression of S2 subunit induced downregulation of interferon-gamma-mediated signaling pathway, regulation of phosphatidylinositol 3-kinase activity, adipocytokine signaling, and insulin signaling pathways. NSP15 upregulated genes reflecting neutrophil degranulation, neutrophil-mediated immunity, oxidative phosphorylation, while NSP16 downregulated S-adenosylmethionine-dependent methyltransferase activity. Of interest, methylated RNA immunoprecipitation sequencing MeRIP-Seq and direct RNA sequencing demonstrated that SARS-CoV-2 RNA contained m6A modifications, whereas SARS-CoV-2 infection increased the expression of methyltransferase-like 3 METTL3 and altered its distribution. Furthermore, manipulation of METTL3 expression impacted SARS-CoV-2 replication [62].Transcriptomic analyses of organoids composed by primary human airway epithelial cells infected with SARS-CoV-2 showed rapid viral replication between 1 and 72 h with host ISG upregulation after 72 h postinfection, whereas previous rhinovirus exposure accelerated ISG induction upon SARS-CoV-2 infection [63]. This study highlights the timing between ISG expression and outcomes of SARS-CoV-2 infection. Analysis of transcriptomes from cell lines A549 and Calu3 infected with SARS-CoV-2, MERS-CoV, or IAV showed that perturbations in genes encoding proteins involved with mitochondrial and autophagy processes were specific for SARS-CoV-2, whereas upregulation of GSK3B could be a potential mechanism by which infection disrupts autophagic flux and contribute to viral replication [64]. Infection of human hepatocyte-derived cellular carcinoma cell line Huh7 with SARS-CoV-2 had a profound effect over transcriptional activity relative to several signaling pathways, whereas further assays confirmed the perturbations of Akt/mTOR/HIF-1 signaling [65]. An assessment of transcriptomes from A549 cells infected with SARS‐CoV‐2 revealed differential expression of genes involved with the mevalonate pathway, which was specific to SARS-CoV-2 infection when compared to infections with H3N2 influenza virus, H1N1 influenza virus, or respiratory syncytial virus [66]. Reanalysis of public transcriptome data from diverse cell lines and organoids infected with SARS-CoV-2 showed the differential expression of several genes involved in glycosylation processes, with significant impact in glycosyltransferases and lectins. This study implicate those molecules as potential factors affecting both viral replication and host response [67].COVID-19 causes more than respiratory symptoms and affects extrapulmonary sites causing intestinal and cardiac manifestations in patients. To understand potential implementation of intracellular pathways during infection of intestinal epithelium, human-induced pluripotent stem cell-derived intestinal organoids HIOs were infected with SARS-CoV-2, which replicated and shed viral particles. Transcriptomics data revealed a robust upregulation of ISGs that was conserved across different epithelial cell types [68]. Transcriptional profiling of primary human cardiac stromal cells derived from cardiospheres demonstrated their susceptibility to SARS-CoV-2 infection, which depended on the expression of ACE2 [69]. These cells also acquired hyperinflammatory and profibrotic phenotypes that could be involved in the pathogenesis of cardiac manifestations. Exposure of human-induced pluripotent stem cell iPSC-derived heart cells to SARS-CoV-2 confirmed productive infection, with concomitant transcriptional signs of damage, especially in cardiomyocytes [70]. Of note, alterations found in this model mimic cytopathic characteristics in hearts of COVID-19 reported studies have contributed to the understanding of processes such as SARS-CoV-2 entry, replication, and host-pathogen interactions. This information enabled the formulation of better models reflecting intracellular pathways activated and repressed upon SARS-CoV-2 infection, whereas tools have been created to facilitate the visualization and evaluation of such pathways. One such tool is the COVID-19 Disease Map, which was generated on previous knowledge from published work and represents a repository for molecular mechanisms of SARS-CoV-2 virus-host interactions [71] and can be used to interrogate transcriptomics data of cells infected with SARS-CoV-2 in vitro as well data obtained from COVID-19 full chapterURL and the Cardiovascular SystemSubramani Mani MBBS, PhD, Mark E. Garcia MD, in Textbook of SARS-CoV-2 and COVID-19, 2024Direct Infection of the MyocardiumDirect entry of SARS-CoV-2 into cells is facilitated by the affinity of the viral spike protein S to the host cell ACE2 receptor, with the host protease transmembrane protease serine 2 TMPRSS2, acting as the Many organs and tissues of the body express both ACE2 and TMPRSS2, including the lungs, heart, gut, liver, kidney, neurons, joints, and eye,39–42 and this explains the tropism and potential of the virus to cause injury to these organs and tissues. Moreover, Chen et showed that although the expression levels of ACE2 are lower in the heart compared with the gut and kidney, the levels were higher in the heart than in the lungs, which act as the primary targets for presents the ACE2 receptor expression profile in the cardiovascular studies and case reports have demonstrated the presence of SARS-CoV-2 genomic RNA or viral particles morphologically identified as SARS-CoV-2 in myocardial tissue obtained from biopsy-confirmed myocarditis Tavazzi et reported one of the earliest cases of biopsy-proven myocardial localization of viral particles with the morphology of a coronavirus in a COVID-19 patient who presented with cardiogenic shock. Escher et identified SARS-CoV-2 genomic RNA in 5 of 104 endomyocardial biopsy EMB samples of patients with suspected myocarditis or unexplained A more recent study by Bearse et looked at 41 consecutive autopsies of patients who died from COVID-19 to understand the relationship of myocardial injury to SARS-CoV-2 infection. Based on in situ hybridization ISH and NanoString transcriptomic NST profiling, the researchers determined that endomyocardial infection by SARS-CoV-2 was present in 30 of 41 cases 73%.20 Cellular targets for SARS-CoV-2 include cardiomyocytes, pericytes, fibroblasts, and resident macrophages of the provides additional details of the mechanism of SARS-CoV-2 entry into the heart and blood on ISH, NST profiling for virus positivity and histopathological findings of inflammatory infiltrates characteristic of myocyte injury for defining myocarditis, the researchers partitioned their study sample n = 41 in three groups—virus-positive with myocarditis n = 4, virus-positive without myocarditis n = 26, and virus-negative without myocarditis n = 11 to study the relationship between cardiac pathological changes and cardiac infection by the SARS-CoV-2 presents the details of the pathological findings in the various groups. Electrocardiographic ECG abnormalities in the form of atrial fibrillation, premature atrial complexes, prolongation of QTc, and nonspecific ST segment and T wave alterations were observed disproportionately in patients whose hearts were infected with et in their histopathological study of 40 patients hospitalized with COVID-19 who subsequently died, report that SARS-CoV-2 RNA was much more prevalent in the lung tissue 34/40 [85%] compared with cardiac tissue 8/40 [20%]45Read full chapterURL Cellular Phagocytosis and Its Impact on Pathogen ControlStefan S. Weber, Annette Oxenius, in Antibody Fc, 2014Targeting of Viruses to FcRsViral infection of target cells in the absence of virus-specific antibodies is in general dependent on the interaction between viral spike proteins and corresponding receptors on target cells, thereby conferring a specific tropism of individual viruses to their target cells. Antibody-opsonized virus particles, however, may gain access to additional FcR-expressing target cells. Uptake of opsonized virus particles into FcR-bearing phagocytes via FcR-dependent phagocytosis may have different outcomes for the infection process and for the ensuing spread and control of the virus infection. While very little is known about the exact intracellular fate of opsonized virus particles and how this relates to their infectivity in phagocytes, most available data indicate that FcR-mediated uptake into phagocytes does not interfere with intracellular viral replication. However, in situations when opsonizing antibodies have direct neutralizing effects on the fusion or uncoating process of the virus, and when this property is maintained under acidic conditions as present in late phagosomes/lysosomes,106–108 FcR-mediated uptake of opsonized viruses might restrict replication within phagocytes. In cases where the infected phagocyte does not support the requirements of a specific viral life cycle, FcR-mediated uptake of opsonized viruses may also lead to enhanced control of viral full chapterURL coronavirus disease COVID-19 Emergence, early infection rate, and deployment strategies for preventive solutionsMohona Munshi, ... Sourav Chakraborty, in Lessons from COVID-19, CurcuminIt is a natural polyphenolic compound that can be used as a potential treatment for COVID-19 patients. The preliminary for COVID infection is interaction with the human cell and viral spike protein. Angiotensin-converting enzyme 2 ACE-2 presents in the human respiratory tract which acts as the receptor is identified by the SARS-CoV-2 spike protein. Then the viral genome RNA is released in the cytoplasm which follows membrane fusion and the RNA codes for instant replication of proteins and transcription complex Jia et al., 2005. After entering the cell, the CoV enables the expression of gene and encoding of genome ensues. This will again in turn encode the accessory protein which allows the adaption of CoV to the human host. This curcumin can restrain the virus entry to the cell, prevent the virus encapsulation and viral protease, and modulate different cell signaling pathways. Curcumin has various antiviral activities and is a therapeutic choice for the management of COVID-19 infection. Curcumin can modulate several molecular targets that get attachment and internalization of SARS-CoV-2 in various organs including the kidney and liver. Curcumin can modulate cellular signals such as apoptosis, inflammation, and RNA replication. It also suppresses pulmonary edema and fibrosis associated with the pathway of COVID-19 infection. But the bioavailability of curcumin is less which can only be mitigated by the administration of nontoxic limits. Overall, the immunomodulatory and antiinflammatory effects show evidence of the antifibrotic and pulmonary protective nature of this phytochemical on lung tissue making it a potential way of COVID-19 treatment Zahedipour et al., 2020.Read full chapterURL Fenner's Veterinary Virology Fifth Edition, 2017Virus ReplicationArenaviruses replicate noncytolytically to high titer in many kinds of cells, including Vero African green monkey and BHK-21 baby hamster kidney cells. Virus replication occurs in the cytoplasm. The viral spike glycoprotein attaches to a cell receptor, which can be transferrin receptor 1 for several New World arenaviruses and alpha-dystroglycan for lymphocytic choriomeningitis virus. Entry and endosomal uptake occur via either clathrin-dependent or clathrin-independent pathways, perhaps depending on the individual species of arenavirus. Specifically, it is proposed that New World arenaviruses such as Junin virus utilize clathrin-mediated endocytosis, whereas Old World arenaviruses such as lymphocytic choriomeningitis and Lassa viruses utilize a clathrin-independent pathway. Because the genome of the single-stranded, negative-sense RNA viruses cannot be translated directly, the first step in replication is activation of the virion RNA polymerase transcriptase. The ambisense coding strategy of the arenavirus genome means that only the nucleoprotein N and polymerase L protein mRNAs are transcribed directly from genomic RNA before translation Fig. Newly synthesized polymerase and nucleocapsid proteins facilitate the synthesis of full-length, complementary-sense RNA, which then serves as template for the transcription of glycoprotein GP and zinc-binding protein Z mRNAs and the synthesis of more full-length, negative-sense RNA. Budding of virions occurs from the plasma membrane Fig. Arenaviruses have limited ability to lyse the cells in which they replicate, usually producing a carrier state in which defective-interfering particles are produced see Chapter 2 Virus Replication. After an initial period of active virus transcription, translation, genome replication, and production of progeny virions, viral gene expression is downregulated, and cells enter a state of persistent infection wherein virion production continues for an indefinite period but at a greatly reduced rate providing a mechanism for persistent nonlethal infection of potential reservoir hosts Table Budding of Lujo virus from the plasma membrane of an infected Vero of C. Goldsmith, C. Humphrey, B. Bird, Centers for Disease Properties of ArenavirusesTwo genera, Mammarenavirus and Reptarenavirus, with two historical subgroups of mammalian viruses, one for Old World and one for New World mammarenaviruses. Reptarenaviruses are associated with snakesVirions are pleomorphic, enveloped, 50–300 generally 110–130 nm in sizeVirion contains nonfunctional host-cell ribosomesVirions contain at least two circular helical nucleocapsids with associated RNA-dependent RNA polymerase transcriptaseGenome consists of two segments, large L, kb and small S, kb, of single-stranded RNA, both ambisenseViral proteins nucleoprotein N, RNA-dependent RNA polymerase L, two glycoproteins Gp1, Gp2, and a zinc-binding matrix protein ZReplication occurs in the cytoplasm; generally noncytocidal; persistent infectionsMaturation occurs by budding from the plasma membraneGenetic reassortment occurs between closely related virusesRead full chapterURL of Protein SynthesisHenry Wade, ... Qiaozhu Su, in Advances in Protein Chemistry and Structural Biology, 2022AbstractSevere acute respiratory syndrome coronavirus 2 Sars-CoV-2 has caused a global pandemic that has affected the lives of billions of individuals. Sars-CoV-2 primarily infects human cells by binding of the viral spike protein to angiotensin-converting enzyme 2 ACE2. In addition, novel means of viral entry are currently being investigated, including Neuropillin 1, toll-like receptors TLRs, cluster of differentiation 147 CD147, and integrin α5β1. Enriched expression of these proteins across metabolic regulatory organs/tissues, including the circulatory system, liver, pancreas, and intestine contributes to major clinical complications among COVID-19 patients, particularly the development of hypertension, myocardial injury, arrhythmia, acute coronary syndrome and increased coagulation in the circulatory system during and post-infection. Pre-existing metabolic disease, such as cardiovascular disease, obesity, diabetes, and non-alcoholic fatty liver disease, is associated with increased risk of hospitalization, persistent post-infection complications and worse outcomes in patients with COVID-19. This review overviews the biological features of Sars-CoV-2, highlights recent findings that delineate the pathological mechanisms of COVID-19 and the consequent clinical full chapterURL RhabdovirusesH. Bourhy, ... Boyle, in Encyclopedia of Virology Third Edition, 2008Virion PropertiesMorphologyRhabdovirus virions are 100–400 nm long and 50–100 nm in diameter Figure 1. Viruses appear bullet-shaped. From the outer to the inner side of the virion, one can distinguish the envelope covered with viral glycoprotein spikes and, internally, the nucleocapsid with helical symmetry consisting of the nucleoprotein tightly bound to genomic Organization and GeneticsAll rhabdoviruses contain a genome consisting of a nonsegmented single-stranded negative-sense RNA molecule with a size in the range of approximately kbp. This RNA molecule contains at least five open reading frames ORFs encoding five virion proteins in the order 3′–5′ nucleoprotein N; phosphoprotein P; matrix protein M; glycoprotein G; and polymerase L. Viruses in the genus Ephemerovirus contain several additional ORFs between the G and L genes, which encode a second glycoprotein GNS and several other nonstructural proteins. Similarly, in the genus Novirhabdovirus, a sixth functional cistron between the G and L genes encodes a nonstructural protein NV of unknown function. The unclassified rhabdoviruses, sigma virus infecting flies Drosophila spp. and plant rhabdoviruses in the genera Cytorhabdovirus and Nucleorhabdovirus also contain an additional ORF which is located between the P and M genes. Flanders virus from mosquitoes Culista melanura has a complex arrangement of genes and pseudogenes in the same genome region. Nucleotide sequence analysis of Tupaia virus from the tree shrew Tipiai belangeri has identified an additional gene encoding a small hydrophobic protein between the M and G genes, and genome sequence analysis of Wongabel virus, an unassigned rhabdovirus isolated from biting midges Culicoides austropalpalis, has revealed that it contains five additional genes that appear to be novel. The function of these other proteins including additional glycoproteins is not yet known. Therefore, despite preservation of a characteristic particle morphology, the Rhabdoviridae includes viruses that display a wide genetic diversity Figure 2.Figure 2. Genome organization of low sequence identities across the Rhabdoviridae prevent the construction of a family phylogeny. One approach to determining the phylogenetic relationships among the rhabdoviruses, as well as the identification of new viral species, is to utilize the conserved regions that have been identified in alignments of the N and L full chapterURL Methods in Protein Biochemistry Part CSabyasachi Baboo, ... John R. YatesIII, in Methods in Enzymology, N-glycosylated viral spike proteins as vaccine candidatesViruses account for at least one fifth of all communicable diseases Collaborators, 2018; Fauci, Touchette, & Folkers, 2005; Gaunt, Harvala, McIntyre, Templeton, & Simmonds, 2011; Jones et al., 2008; Wolfe, Dunavan, & Diamond, 2007; Woolhouse, Scott, Hudson, Howey, & Chase-Topping, 2012 and are responsible for vast economic losses Smith, Machalaba, Seifman, Feferholtz, & Karesh, 2019 and human suffering Mayer, Shisana, & Beyrer, 2016. For decades, scientists have studied the mechanisms of how viruses are recognized by hosts and how they escape host immune systems Chan & Gack, 2016; Dimitrov, 2004; Freed & Martin, 1995; Marsh & Helenius, 2006; Thompson, de Vries, & Paulson, 2019, and they have used this knowledge to guide the design of vaccines against viral pathogens Harvey et al., 2021; Seabright, Doores, Burton, & Crispin, 2019; VanBlargan, Goo, & Pierson, 2016. Because viral spike proteins or peplomers are responsible for viral anchorage and entry into host cells Dimitrov, 2004; Freed & Martin, 1995; Marsh & Helenius, 2006, they are the prime antigenic target for vaccines. However, these proteins help the virus evade the host immune system through heavy glycosylation Seabright et al., 2019 and heterogeneity of their glycoforms Rudd & Dwek, 1997; Zhang, Li, Lu, & Liu, 2017, so glycosylation patterns must be considered in vaccine design Burton & Hangartner, 2016; Seabright et al., 2019; Steichen et al., 2019; Thompson et al., 2019. What we know about glycosylation of viral spike proteins has come primarily from experiments in cultured cells and does not include information about the variations induced by proteotoxic stress in virus-infected cells Boyce & Yuan, 2006; Hirschberg et al., 1998; Hossler, Mulukutla, & Hu, 2007; Kaufman, 1999; Su, Liao, & Lin, 2002; Sun, Tie, Chen, & Lu, 2020; Wong et al., 2018; Yeo, Parent, Yeo, & Olden, 1985, phenotypic shifts in virus reproduction driven by interactions with the immune system Phillips, Doud, et al., 2018; Phillips, Ponomarenko, et al., 2018 or natural variations in glycosylation created by growth in different cell types Kong et al., 2010; Pritchard, Harvey, Bonomelli, Crispin, & Doores, 2015; Raska et al., 2010; Wang et al., 2020; Zhao, Song, Huang, Yu, & Mechref, 2021. The use of viral spike proteins derived directly from infected individuals would more accurately represent glycan heterogeneity and in vivo host-pathogen interactions for the design of vaccines. However, clinical samples are available in limited supply, and thus provide only very small quantities of viral spike glycoproteins. The sensitivity of existing approaches for analyzing site-specific glycan heterogeneity makes the analysis of such small quantities of glycoprotein full chapterURL spike pada virus tersusun atas protein dan karbohidrat yang disebut...1. spike pada virus tersusun atas protein dan karbohidrat yang disebut...2. spike pada virus tersusun atas protein dan karbohidrat yang disebut3. spike virus tersusun atas protein dan kharbohidrat yng disebut4. Susunan dinding sel jemur terdiri atas karbohidrat dan protein yang disebut5. kapsid virus tersusun atas subunit-subunit protein yang disebut6. virus tersusun atas selubung protein yang disebut ?7. Virus tersusun atas selubung protein yang disebut ...... 8. Virus tersusun atas selubung protein yang disebut..9. Virus tersusun atas selubung protein yang disebut ....... 10. virus tersusun atas selubung protein yang di sebut 11. virus tersusun atas selubung protein yang disebut ....12. sebutkan unsur penyusun karbohidrat, lemak, dan protein13. Virus tersusun atas lubang protein yg di sebut14. sebutkan 3 unsur protein yang sama dengan penyusun karbohidrat15. sebutkan unsur penyusun karbohidrat, lemak, dan protein16. selubung virus tersusun atas... a. protein b. asam inti c. lemak d. karbohidrat e. RNA17. Virus tersusun atas selubung protein yang disebut apakah?18. Kapsid virus tersusun atas subunit subunit protein yqng di sebut19. Selubung virus yang tersusun atas molekul protein disebut 20. Virus tersusun atas selubung protein yang disebut dengan uraian.... [tex] Sitologi, Virologi [/tex]Protein dan karbohidrat akan menyatu membentuk komponen lipopolisakarida. Lipopolisakarida ini dapat menyusun spike virus dibawah tabung virus. 2. spike pada virus tersusun atas protein dan karbohidrat yang disebut Spike pada virus tersusun atas protein dan karbohidrat yang disebut Kapsid 3. spike virus tersusun atas protein dan kharbohidrat yng disebut glikoprotein atau glikopeptidaJawaban Glikoprotein Glikopeptida . . . 4. Susunan dinding sel jemur terdiri atas karbohidrat dan protein yang disebut Kitin 5. kapsid virus tersusun atas subunit-subunit protein yang disebut RNAribo nukleat acid atau DNAdeoksiribo nukleat acid 6. virus tersusun atas selubung protein yang disebut ? selubung protein disebut kapsid 7. Virus tersusun atas selubung protein yang disebut ...... SoalVirus tersusun atas selubung protein yang disebut ......Jawaban dengan penjelasanKapsidVirus memiliki struktur tubuh yang sangat sederhana. Virus hanya memiliki satu macam materi genetik yang dikelilingi oleh suatu protein pelindung yang disebut kapsid. Sehingga, selubung protein pada virus dinamakan kapsid. Bukaanmaen 8. Virus tersusun atas selubung protein yang disebut.. kapsid gan bentukny juga beragamDNA atau RNA yang dikelilingi oleh suatu protein pelindung yang disebut kapsid. 9. Virus tersusun atas selubung protein yang disebut ....... Jawabankapsid atau capsidsPenjelasansemoga membantu 10. virus tersusun atas selubung protein yang di sebut selubung protein kapsidvirus hanya tersusun atas selubung kapsid selubung kapsid yang tersusun oleh molekul protein. 11. virus tersusun atas selubung protein yang disebut .... selubung protein disebut kapsitnama selubung protein penyusun virus adalah kapsid 12. sebutkan unsur penyusun karbohidrat, lemak, dan protein KarbohodratC. H. OLemakC. H. OProteinC. H. O. N. Kadang ada S. PC karbonH hidrigenO oksigenN nitrogenS sulphurP phospat 13. Virus tersusun atas lubang protein yg di sebut KapsidKamis 13-12-2018 14. sebutkan 3 unsur protein yang sama dengan penyusun karbohidrat 3 unsur tersebut yaitu karbon C, oksigen O serta hidrogen H 15. sebutkan unsur penyusun karbohidrat, lemak, dan protein -unsur penyusun karbohidrat adalah Karbon C, Hidrogen H dan Oksigen O.-unsur penyusun lemak adalah Karbon C, Hidrogen H dan Oksigen O.-unsur penyusun protein adalah Karbon C, Hidrogen H, Oksigen O, dan Nitrogen N. Terkadang protein juga mengandung unsur Posfor P dan Sulfur S 16. selubung virus tersusun atas... a. protein b. asam inti c. lemak d. karbohidrat e. RNA kalau memurutku jwbannya e. RNA 17. Virus tersusun atas selubung protein yang disebut apakah? virus terbungkus oleh selubung protein yang disebut kapsid 18. Kapsid virus tersusun atas subunit subunit protein yqng di sebut kapsomer....................Terbuat dari protein yang disebut protomerSemoga membantu ya 19. Selubung virus yang tersusun atas molekul protein disebut AnsSelubung pada virus yang tersusun atas molekul protein disebut selubung selubung sebagai pelindung genome virussemoga membantu. 20. Virus tersusun atas selubung protein yang disebut dengan uraian.... Virus tersusun atas selubung protein yang disebut dengan uraian membantu.

spike pada virus tersusun atas protein dan karbohidrat yang disebut