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The detection of virus coded proteins in cauliflower mosaic virus infected plants and protoplastsHarker, C. L. January 1987 (has links)
No description available.
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Selection of chicken single-chain antibody fragments directed against recombinant VP7 of bluetongue virusRakabe, Molemaisago Magdeline 17 February 2009 (has links)
Viral protein seven (VP7) is a major core protein and a group-reactive antigen that can be used for the diagnosis of bluetongue virus. VP7 gene of bluetongue virus serotype 4 was expressed in E. coli. Using phage display technology, anti-VP7st4 scFvs were selected from a chicken scFv library (Nkuku®) following different panning strategies. Polyclonal phage ELISA showed that VP7st4-specific scFvs were enriched after three rounds of panning. Six different scFvs (A1, H2, TA8, TC9, TD12 and SA12) were identified by sequence analysis. Stability of these scFvs was determined by incubation at different temperatures and after several freeze/thaw cycles. The scFvs were also tested in an inhibition ELISA. Inhibition with an anti-bluetongue virus guinea pig serum resulted in a 30% decrease in ELISA signal of A1. No inhibition was obtained with the rest of the scFvs when guinea pig and sheep serum were used. An anti-bluetongue virus chicken IgY inhibited the scFvs by 50% to 86%. A fragmented-gene library displaying peptides of VP7st4 was constructed. The library was subjected to three rounds of affinity selection against the anti-VP7st4 scFvs. Enrichment of clones specific to each scFv was observed. The clones were identified by sequence analyses. The regions on VP7st4 to which the scFvs bind could not be identified since no duplicate clones were selected. / Dissertation (MSc)--University of Pretoria, 2008. / Veterinary Tropical Diseases / unrestricted
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Analysis of the Cytopathogenic Effect of Different HIV-1 Vpr Isoforms on Primary Human CD4+ T Cells and a Model Cell LineFierro Nieves, Jonatan Josue 13 September 2022 (has links)
Human Immunodeficiency Virus (HIV) is the causal agent of acquired immunodeficiency syndrome (AIDS), a disease characterized by the depletion of CD4+ T cells which impairs immune response. Analysis of HIV-1 infected patients has identified two distinctive phenotypes that differ in length of time towards the development of AIDS, Rapid Progressor (RP) and Long-Term Non-Progressor (LTNP) patients. The cause of the differences between these two groups is a process that is still under investigation. Hints about a possible cause have been attributed to the discovery of mutations in the viral protein R (Vpr) that have been associated with these phenotypes: mutations producing the isoforms R36W to RP patients and R77Q to LTNP patients. It has been suggested that these mutations play an important role in the depletion of CD4+ T cells, however more studies are needed to clarify and support this idea. This study examines the effect of the two isoforms in the infection of human primary CD4+ T cells and a model cell line, using the viral strain HIV-1 JR-CSF and derived strains to which the aforementioned mutations have been induced. Our results show that after infection, isoform R77Q has the capacity to significantly induce more apoptosis (identified by Annexin V staining) than Vpr wild type (WT) and the viral strain expressing the isoform R36W. Moreover, R36W significantly induces more cell death by necrosis than R77Q. Notably, the differences found in the way these isoforms of Vpr induce necrosis and apoptosis support the idea of the correlation between strains harboring these mutations and the phenotypes of RP and LTNP patients.
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The cellular chloride channels CLIC1 and CLIC4 contribute to virus-mediated cell motilityStakaityte, G., Nwogu, N., Lippiat, J.D., Blair, G.E., Poterlowicz, Krzysztof, Boyne, James R., Macdonald, A., Mankouri, J., Whitehouse, A. 02 August 2018 (has links)
Yes / Ion channels regulate many aspects of
cell physiology, including cell proliferation,
motility, and migration, and aberrant expression
and activity of ion channels is associated with
various stages of tumor development, with K+
and Cl- channels now being considered the most
active during tumorigenesis. Accordingly,
emerging in vitro and preclinical studies have
revealed that pharmacological manipulation of
ion channel activity offers protection against
several cancers. Merkel cell polyomavirus
(MCPyV) is a major cause of Merkel cell
carcinoma (MCC), primarily due to the
expression of two early regulatory proteins
termed small and large tumour antigens (ST and
LT, respectively). Several molecular
mechanisms have been attributed to MCPyVmediated
cancer formation but thus far, no
studies have investigated any potential link to
cellular ion channels. Here we demonstrate that
Cl- channel modulation can reduce MCPyV STinduced
cell motility and invasiveness.
Proteomic analysis revealed that MCPyV ST
upregulates two Cl- channels; CLIC1 and CLIC4,
which when silenced, inhibit MCPyV STinduced
motility and invasiveness, implicating
their function as critical to MCPyV-induced
metastatic processes. Consistent with these data,
we confirmed that CLIC1 and CLIC4 are
upregulated in primary MCPyV-positive MCC
patient samples. We therefore, for the first time,
implicate cellular ion channels as a key host cell
factor contributing to virus-mediated cellular
transformation. Given the intense interest in ion
channel modulating drugs for human disease,
this highlights CLIC1 and CLIC4 activity as
potential targets for MCPyV-induced MCC. / BBSRC DTP studentship (BB/J014443/1) and Royal Society University Research Fellowship to JM (UF100419)
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Divalent Copper Compounds as Inhibitory Agents of Influenza AGordon, Nathan Allan 01 June 2014 (has links)
Influenza A virus (IAV) exhibits a high mutation frequency. Mutations in primary viral targets such as hemagglutinin, neuraminidase, and the proton channel M2 have afforded IAV with substantial drug resistance to previously effective drugs such as oseltamivir and amantadine (AMT) along with their analogs. One of the main drug-resistant alterations in the M2 protein that has become ubiquitous is the mutation S31N. Divalent copper has previously been suggested to have anti-IAV properties using in vitro assays involving Xenopus oocytes and SSNMR. In this work, the EC50 of AMT, two AMT analogs, CuCl2 · 2H2O, and four previously published Cu2+ complexes were tested for antiviral activity against the California/07/2009 (H1N1) IAV strain containing the S31N M2 protein in viral mini-plaque assays. AMT, CuCl2 · 2H2O, and two previously published divalent copper complexes were tested for M2 proton-transport blocking efficacy in liposomes using truncated M2 (22-62, S31N). Two novel divalent copper species, NAG101 and NAG107, both derived from AMT analogs were developed and tested for both antiviral activity and M2 blocking efficacy. Cell integrity was maintained at concentrations up to 1 mM (48 hours of exposure) with all compounds except Cu(II) 3. In the viral mini-plaque assay the novel divalent copper complexes NAG101 (EC50 25.7 +/-7.7 µM) and NAG107 (EC50 2.91 +/- 0.29 µM) were 2.5-fold and 21-fold better than AMT (EC50 64.3 +/- 9.3 µM) respectively. In the liposome assay NAG101 (EC50 18.9 +/- 1.5 µM) and NAG107 (EC50 4.5 +/- 0.6 µM) were 2.5-fold and 11-fold better than AMT (EC50 49.3 +/- 2.9 µM respectively. In the viral mini-plaque assay, CuCl2 · 2H2O (EC50 57.2 +/- 10.1 µM) was comparably effective to AMT, but was more than ten times more effective in the liposome assay targeting S31N M2 with an EC50 6.1 +/- 0.8 µM. Divalent copper species possess anti-IAV activity against the ubiquitous S31N M2-containing viral strain California/07/2009 (H1N1) and may prove to be effective against other IAV strains by blocking M2.
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Studies On The Structural And Biological Properties Of Rotavirus Enterotoxigenic Non-structural Protein 4 (NSP4)Palla, Narayan Sastri 06 1900 (has links) (PDF)
Rotavirus is the major cause of infantile gastroenteritis. Each year more than 600,000 young children are estimated to die in developing countries throughout the world. Rotavirus infection can be either symptomatic or asymptomatic. But the genetic or molecular basis for rotavirus virulence is not yet clearly understood. NSP4, encoded by genome segment 10, is a multifunctional protein. It is identified as the first viral enterotoxin and is essential for virus morphogenesis and pathogenesis. Analysis of NSP4 from more than 175 strains failed to reveal any sequence motif or amino acid that segregated with the virulence phenotype of the virus. Further, a few studies indicated a lack of consistent correlation between virus virulence and diarrhea inducing ability of the cognate NSP4.
To understand the basis for the inconsistency in the enterotoxigenic activity of a few NSP4s reported in a limited number of studies, comparative analysis of the biophysical, biochemical, and biological properties of NSP4ΔN72, which from SA11 and Hg18 was earlier shown to be highly diarrheagenic, from 17 different symptomatic and asymptomatic strains was carried out. To study structure-function relationship we used Thioflavin T fluorescence assay, gel filtration, CD spectroscopy, trypsin susceptibility and enterotoxin assay in newborn mice for all the proteins. Detailed comparative analysis of biochemical and biophysical properties and diarrheagenic activity of the recombinant ΔN72 peptides under identical conditions revealed wide differences among themselves in their resistance to trypsin cleavage, thoflavin T binding, multimerization and conformation without any correlation with their diarrhea inducing abilities. Since earlier studies showed that a secreted peptide (ΔN112) of SA11-NSP4 also induced diarrhea in newborn mice pups, we have generated NSP4ΔN112 deletions from six different strains and tested for their diarrhea inducing ability. The patterns of DD50 values of the ΔN112 peptides was similar to that for ΔN72 peptides, but were 1000-1200-fold less efficient than that of SA11ΔN72.
NSP4 exists in multiple forms in the infected cells- as oligomers, higher molecular weight complexes and ER- and cytoplasmic membrane anchored forms. Previous studies suggest that the N-terminal boundary of the oligomerization domain could lie downstream to residue 94 from the N-terminus. A peptide from residue 112-175, secreted from rotavirus infected cells, was reported to induce dose-dependent diarrhea in suckling mice, suggesting that the N-terminal boundary of the enterotoxin activity could lie around residue 112. However, the precise N-terminal boundaries in NSP4 for oligomerization and diarrhea induction have not been identified. To address this question, a large number of deletion mutants C-terminal to residue 94 were generated and tested for their ability to induce diarrhea in newborn mouse pups. Our data suggest that while the deletions ∆N121 to ∆N131 failed to induce diarrhea, ΔN118 was diarrheagenic suggesting that the N-terminal boundary of the minimal diarrhea inducing domain lies between aa 118 and 121. Size exclusion chromatography revealed that residues 95 to 98 are critical and sufficient for oligomerization. Studies on oligomerization further revealed that NSP4ΔN94 exists in pentamers, tetramers and dimers, while deletion mutants C-terminal to aa 94 exist only as dimers. Our studies demonstrate for the first time that not only tetramers but pentamers as well as dimers possess enterotoxigenic properties.
Most human rotavirus infections are caused by group A rotaviruses. Within this group, rotaviruses are further classified into subgroups based on the antigenic specificity associated with the protein product of the sixth gene, VP6. Previous studies have mapped SG I specificity to aa position 305 and the region between 296 and 299, and SG II specificity to residue 315 on VP6. However, the subgroup specific determinants on NSP4 have not been identified till date. In this study, we generated several amino acid substitution mutants in the SG I-specific SA11 NSP4∆N72 protein as in previous studies ∆N72 was found to efficiently bind DLPs. Using an enzyme linked immunosorbent assay method, the effect of the mutations in the C-terminal and N-terminal regions in ∆N72 on their binding ability to SG I and SG II DLPs was assayed. Residues at positions 85, 169, 174 and 175 and in the ISVD appear to collectively determine the specificity of binding to DLPs. While the conserved proline and glycines at positions 165, 168 and 162, respectively, are important for maintaining the required conformation for general recognition of DLP. The present study provides important insights towards understanding the determinants in NSP4 for SG-specific DLP interaction.
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Characterization Of A Bovine Rotavirus From Humans And Studies On The Structural And Biological Properties Of Rotaviral Enterotoxigenic Nonstructural Protein 4Jagannath, M R 06 1900 (has links) (PDF)
No description available.
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Changes in RNA Expression of HuT78 Cells Resulting From the HIV-1 Viral Protein R R77Q MutationRamsey, Joshua S. 24 October 2023 (has links) (PDF)
Human immunodeficiency virus type 1 (HIV-1) is the causative virus for acquired immunodeficiency syndrome (AIDS). AIDS is characterized by chronic inflammation and reduction of CD4+ T-cells in the blood. This leads to the patient becoming immunocompromised and much more susceptible to disease in general. Different phenotypes in the progression of AIDS have been observed in patients in either progressing to AIDS faster as a Rapid Progressor (RP), or slower as a Long-Term Non-Progressor (LTNP). Researching elements that result in the LTNP phenotype is of interest as it has the potential to offer alternative treatments and therapies to those suffering from HIV and improve their quality of life. A separate genome wide association study into a population of LTNP patients had associated the R77Q mutation of viral protein R with the LTNP phenotype. Although this association has been controversial, recent work has shown that the R77Q mutation promotes apoptosis in a variety of cell lines compared to unmutated virus. However, the mechanisms behind the increase in apoptosis remain a place for further research. In this thesis, we attempted to elucidate some of the exact changes in gene expression between cells infected with the R77Q mutation and those without in the induction of apoptosis. We observed that apoptosis could be detected approximately 24 hours after infection via Annexin V staining, but there were no significant differences in the expression of genes within the first 24 hours. Furthermore, we observed 289 genes were then differentially expressed at 72 hours post infection. Analysis through SPIA revealed that the c-myc transcription factor pathway was activated in the R77Q infected cells and further analysis of the individual genes suggested less inflammatory signals in R77Q populations as well as an overall increase in antiapoptotic genes in WT infected cells. Exploration into the ANT1, Bax, and B-cl2 genes revealed that B-cl2 was upregulated in WT HIV infections and provided a degree of protection from apoptotic processes. Differences found in the expression of genes between R77Q and WT infected cells support the observation of increased apoptosis in R77Q infections and identify several targets for further research into the LTNP phenotype.
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Characterization Of Structural And Non-structural Proteins Of Positive Sense, Single-stranded RNA Plant VirusesMathur, Chhavi 06 1900 (has links) (PDF)
In the present thesis, two positive sense single-stranded RNA viruses have been used as models to understand the structure and function of viral-encoded proteins. One of them, Pepper Vein Banding Virus (PVBV; genus Potyvirus; family Potyviridae) is a flexuous, rod-shaped virus that encodes for a polyprotein of size ~340 kDa. The polyprotein undergoes proteolytic processing by viral-encoded proteases, of which Nuclear Inclusion-a Protease (NIa-Pro) is the major protease. It is a serine-like cysteine protease which cleaves between a Q/A or Q/S, present in the context of the heptapeptide recognition sequence. The temporal regulation of intermediates and mature proteins released by NIa-Pro cleavage is crucial for a successful infection. In the present study, histidine-tagged NIa-Pro, Viral Protein genome-linked (VPg), and the cleavage site mutant (E191A) VPg-Pro were over-expressed in E. coli and purified. The protease activity of NIa-Pro was monitored using an HPLC-based protease assay developed using a peptide substrate. NIa-Pro protease activity was found to get modulated upon interaction with VPg and upon undergoing phosphorylation. Both these events have been found to involve the face of NIa-Pro which contains the solvent-exposed Trp143. Mutational studies and molecular dynamics analyses provide evidence that this residue is buried upon interaction of NIa-Pro with VPg, and any perturbation of its orientation influences the active site Cys151 via an extensive interaction network. This interaction was found to enhance the velocity of NIa-Pro protease activity, especially if the two domains were present in trans (VPg+Pro). In addition, the main-chain –NH2 group of Trp143 was found to be hydrogen-bonded to the side chain –OH group of Ser129, the residue which was identified to undergo phosphorylation by host plant kinases. Interestingly, when the two domains were present in cis (E191A VPg-Pro), no phosphorylation was observed. Mutations of Ser129 (to phosphorylation-mimic Asp or phosphorylation-deficient Ala residues) which affected this H-bond were found to disturb Trp143 and Cys151 orientation, which drastically reduced the protease activity of NIa-Pro. Within the polyprotein, VPg is present at the N-terminus of NIa-Pro and the cleavage site between them is suboptimal (E/A). In the present study, VPg-Pro was shown to be covalently linked to the genomic RNA present in the virions. Interestingly, during purification, VPg could only be purified from the soluble when it was expressed at the N-terminus of NIa-Pro. A series of bioinformatics and biophysical analysis of VPg showed that PVBV VPg, like other potyviral VPgs, exists as a molten-globule. Moreover, while VPg was shown to harbour the Walker motifs, it was found to exhibit an ATPase activity only when it was present with the NIa-Pro (especially in cis). Lys47 and Asp88:Glu89 were found crucial for optimal activity. Over all the results demonstrated that there is a reciprocal modulation of structure and function of the VPg and NIa-Pro domains. These results can explain the possible significance of an impeded cleavage rate between the two domains of VPg-Pro during PVBV infection. The precursor, VPg-Pro, could offer the advantage of evading the inhibitory phosphorylation of NIa-Pro by the host, as well as drive certain viral processes by virtue of its ATPase activity. And subsequent cleavage of the domains and their trans interaction could offer a higher turnover rate which might assist sufficient CP production required for viral morphogenesis. Another virus, Tobacco Streak Virus (TSV) that belongs to the Ilarvirus genus of the Bromoviridae family is a spherical virus which forms pleiomorphic icosahedral virus particles. It has a tripartite genome and each RNA is encapsidated individually. In the present thesis, TSV was used as a model to understand the properties of its structural protein-the coat protein (CP), with the aim of deciphering TSV assembly process. Thus, the CP gene from TSV RNA 3 was cloned and over-expressed in E. coli. The coat protein thus expressed formed virus-like particles (VLPs), which could be disassembled into dimers using high CaCl2 concentrations. Reassembly of VLPs was possible from dimers even in the absence of any nucleic acid. Mutational analysis of the N-terminal disordered domain showed that 26 amino acid residues from the amino-terminus could be crucial for capsid heterogeneity while, zinc-binding domain was essential for assembly. Overall, the present study shows that the flexible W-C loop of PVBV NIa-Pro, the disordered N-terminal region of PVBV VPg and the disordered N-terminal region of TSV CP harbour residues crucial for regulation of protein function. Such regulatory elements would ultimately allow viruses to maintain a smaller protein number, and thus a smaller genome size.
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Mutagenesis and functional studies of the HIV-1 vpr gene and Vpr protein obtained from South African virus strainsRomani, Bizhan 03 1900 (has links)
Thesis (PhD)--University of Stellenbosch, 2011. / ENGLISH ABSTRACT: Background: Human immunodeficiency virus type 1 (HIV-1) viral protein R (Vpr) is
an accessory protein that interacts with a number of host cellular and other viral
proteins. Vpr exerts several functions such as induction of apoptosis, induction of cell
cycle G2 arrest, modulation of gene expression, and suppression of immune
activation. The functionality of subtype C Vpr, especially South African strains, has
not been studied. The aim of this study was to describe the diversity of South African
HIV-1 subtype C vpr genes and to investigate selected functions of these Vpr
proteins.
Methodology: The HIV-1 vpr region of 58 strains was amplified, sequenced, and
subtyped using phylogenetic analysis. Fragments containing natural mutations were
cloned in mammalian expression vectors. A consensus subtype C vpr gene was
constructed and site-directed mutagenesis was used to induce mutations in postions in
which no natural mutations have been described. The functionality of all constructs
was compared with the wild-type subtype B Vpr, by transfecting human 293T cell
line to investigate subcellular localization, induction of apoptosis and cell cycle G2
arrest. The modulation of genes expressed in the induction of apoptosis using TaqMan
Low density arrays (TLDA) was also investigated.
Results: Phylogenetic analysis characterized 54 strains as HIV-1 subtype C and 4
strains as HIV-1 subtype B. The overall amino acid sequence of Vpr was conserved
including motifs FPRPWL and TYGDTW, but the C-terminal was more variable. The
following mutations were constructed using site-directed mutagenesis: P14I, W18C,
Y47N, Q65H and Q88S. Subtype B and all natural mutants of subtype C Vpr
localized to the nucleus but the W18C mutation disturbed the nuclear localization of
Vpr. The cell cycle G2 arrest activity of all the mutants, as well as consensus-C, was
lower than that of subtype B Vpr. All the natural mutants of subtype C Vpr induced
cell cycle G2 arrest in 54.0-66.3% of the cells, while subtype B Vpr induced cell cycle
G2 arrest in 71.5% of the cells. Subtype B and the natural mutant Vpr proteins
induced apoptosis in a similar manner, ranging from 95.3-98.6% of transfected cells.
However, an artificially designed Vpr protein containing the consensus sequences of
subtype C Vpr indicated a reduced ability to induce apoptosis. While consensus-C
Vpr induced apoptosis in only 82.0% of the transfected cells, the artificial mutants of
Vpr induced apoptosis in 88.4 to 96.2% of the cells. The induction of apoptosis associated
gene expression was similar for all constructs, indicated that apoptosis was
efficiently induced through the intrinsic pathway by the mutants.
Conclusion: This study indicated that both HIV-1 subtype B and C Vpr display a
similar ability for nuclear localization and apoptosis induction. The induction of cell
cycle G2 arrest by HIV-1 subtype B Vpr may be more robust than many subtype C
Vpr proteins. The natural mutations studied in the isolates did not disturb the
functions of subtype C Vpr and in some cases even potentiated the protein to induce
apoptosis. Naturally occurring mutations in HIV-1 Vpr cannot be regarded as
defective, since enhanced functionality would be more indicative of an adaptive role.
The increased potency of the mutated Vpr proteins suggests that Vpr may increase the
pathogenicity of HIV-1 by adapting apoptotic enhancing mutations. / AFRIKAANSE OPSOMMING: Agtergrond: Die virus protein R (Vpr) van Menslike Immuungebrek Virus tipe 1
(MIV-1) is ‘n bykomstige protein wat met ‘n aantal sellulêre proteine van die gasheer
en ander virus proteine in wisselwerking tree. Vpr het 'n invloed op verskeie funksies
onder andere die induksie van apoptose, die induksie van selsiklus G2 staking,
modulering van geen uitdrukking en onderdrukking van immuun aktivering. Die
funksionaliteit van subtipe C Vpr, en veral die van Suid-Afrikaanse stamme, is nie
beskryf nie. Die doelwit van die studie was om die diversiteit van Suid Afrikaanse
MIV-1 subtipe C vpr gene te beskryf en ook om selektiewe funksies van die Vpr
proteine te ondersoek
Metodiek: Die MIV-1 vpr streek van 58 stamme is vermeerder, die DNA volgordes is
bepaal en die stamme is gesubtipeer deur filogenetiese analise. Fragmente met
natuurlike mutasies is in ekspressie vektore gekloon. ‘n Konsensus subtipe C Vpr
geen is ontwerp en mutasies in posisies waar geen natuurlike mutasies beskryf is nie,
is ontwerp deur mutagenese. Die funksionaliteit van die konstrukte is met die wilde
tipe subtype B vergelyk deur 293T sellyn te transfekteer en te ondersoek vir
subsellulêre lokalisering, induksie van apoptose, en G2 selsiklus stilstand. Die
modulering van geen uitdrukking in die induksie van apoptose is deur TLDA
ondersoek.
Resultate: Filogenetiese analise het 54 stamme as HIV-1 subtipe C geklassifiseer en
4 stamme as subtype B. Die Vpr aminosuur volgordes was konstant insluitend die
FPRPWL en TYGDTW motiewe, maar die C-terminaal was meer variëerbaar. Deur
mutagenese is die volgende mutasies ontwerp: P14I, W18C, Y47N, Q65H and Q88S.
Subtipe B en al die natuurlike mutante van subtipe C het in die selkern gelokaliseer,
maar die W18C mutasie het die lokalisasie versteur. Die G2 selsiklus stilstand van
alle mutante en konsensus C was laer as die van subtype B. Al die natuurlike subtipe
C mutante het G2 selsiklus tot stilstand gebring in 54.0-66.3% van die selle, terwyl
subtype B selsiklus tot stilstand gebring het in 71.5% van die selle. Subtipe B en die
natuurlike Vpr mutante het apoptose op ‘n soortgelyke wyse geinduseer, wat wissel
tussen 95.3-98.6% van getransfekteerde selle. Die protein met die kunsmatig
ontwerpte konsensus C volgorde het egter ‘n verlaagde vermoë gehad om apoptose te
induseer. Die konsensus subtipe C het apoptose in 82.0% van getransfekteerde selle
geinduseer en die kunsmatige mutante in 88.4 – 96.2% van die selle. Die induksie van
die apoptose verwante geen ekspressie deur die mutante was soortgelyk as die van
konsensus C en subtipe B Vpr wat ’n aangeduiding is dat apoptose effektief
veroorsaak is deur die intrinsieke roete.
Gevolgtrekking: Hierdie studie het aangetoon dat kern lokalisering en apoptose op ‘n
soortgelyke wyse by beide MIV-1 subtipe B en C Vpr plaasvind. Die induksie van
selsiklus G2 stilstand deur MIV-1 subtipe B Vpr is egter meer robuust as baie van die
subtipe C Vpr proteïene. Natuurlike mutasies in MIV-1 Vpr kan nie as gebrekkig
beskou word nie, aangesien beter funksionaliteit 'n aanduiding is vandie aanpasbare
rol. Die verhoogde krag van die gemuteerde Vpr proteïen dui daarop dat Vpr die
patogenisiteit van MIV-1 kan verbeter deur die aanpassing van mutasies.
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