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1                                              KS and NHL diagnoses during 1996 to 2011 were identified
2                                              KS and PEL are aggressive KSHV-associated malignancies w
3                                              KS can develop following organ transplantation through r
4                                              KS incidence rates per 100000 person-years were 52 in th
5                                              KS incidence was lower at 12-23 (IRR = 0.47; 95% CI, .23
6                                              KS is a highly disseminated and vascularized tumor.
7                                              KS risk was 5 times higher in South African women (aHR,
8                                              KS risk was lower in girls than in boys (adjusted HR [aH
9                                              KS spindle cells, the main tumor cells, all contain KSHV
10                                              KS tumors support both latent and lytic KSHV replication
11                                              KS was identified by >/= 1 inpatient or >/= 2 outpatient
12  Over a period of 1066572 person-years, 2046 KS cases were diagnosed.
13                               There were 341 KS cases among 25 529 HIV-infected male veterans (incide
14 ation in RAP1B in a second individual with a KS-like phenotype.
15 mpound 2 for all anions investigated, with a KS/KR ratio of up to 2.
16 , the reduction in insulin sensitivity after KS-oil supplementation was more marked [27% lower than w
17 R gene frequencies in 250 classic (non-AIDS) KS cases, 280 KSHV-seropositive controls, and 576 KSHV-s
18 be an attractive therapeutic target for AIDS-KS.
19 ially effective therapeutic approach in AIDS-KS patients.
20 rtial regression of AIDS-associated KS (AIDS-KS) in five of 10 patients.
21 athogenesis underlying AIDS-related KS (AIDS-KS) remains unknown.
22                   The high incidence of AIDS-KS has been ascribed to the interaction of KSHV and HIV-
23 hogenesis and extensive angiogenesis of AIDS-KS remains unclear.
24 way is important in the pathogenesis of AIDS-KS, which could be an attractive therapeutic target for
25 gressive AIDS-related Kaposi's sarcoma (AIDS-KS) characterized by abnormal angiogenesis.
26 ions of KS, the pathogenesis underlying AIDS-KS remains largely unknown.
27 ernative therapy for some patients with AIDS-KS.
28          In Europe, Latin, and North America KS risk was 6 times higher in men who have sex with men
29                      Activity of the CPS and KS found in this phytopathogen was verified - that is, X
30 ical characterization of the encoded CPS and KS, and the impact of insertional mutagenesis on virulen
31 phosphate and ent-kaurene synthases (CPS and KS, respectively), which are found within a well-conserv
32 ratio and hydrogen bonding between Reb D and KS.
33                                Both KSHV and KS are endemic in sub-Saharan Africa where approximately
34 eir potential role in HHV-8 pathogenesis and KS.IMPORTANCE Here we show that HHV-8, a DNA tumor virus
35           vIL-6 also plays a role in PEL and KS.
36 d the relationship between cART regimens and KS using multivariable Poisson regression, stratified or
37 urene synthase1 (SrKS1) homologs, SrCPS2 and KS-like (SrKSL), which were specifically expressed in tr
38 nical characteristics, overall survival, and KS progression-free survival were analyzed according to
39 her CD4 counts and lower HIV RNA values, and KS occurred more frequently after ART initiation.
40  not pathological aggregates, but rather are KS-WNK1-dependent microdomains of the DCT cytosol that m
41 nduced partial regression of AIDS-associated KS (AIDS-KS) in five of 10 patients.
42 r with aberrant neovascularization caused by KS-associated herpesvirus (KSHV).
43 ciated malignancy is etiologically caused by KS-associated herpesvirus (KSHV).
44 Kgamma were backcrossed into db/+ mice C57BL/KS (>10 generations) to obtain db/db-PI3Kgamma(-/-) mice
45 ation of a protein previously shown to cause KS-like lesions in mice (Rac1), an increase in KS-associ
46 ide Innovations and Technology, Kansas City, KS) designed to protect the head from radiation exposure
47 mmunodeficiency virus (HIV)-negative classic KS cases to plasma from 29 matched controls, using a mul
48 have reported a higher prevalence of classic KS in diabetic patients.
49 istic support for the association of classic KS with diabetes.
50 mumax), nitrite half saturation coefficient (KS), oxygen half saturation coefficient (KO), and biomas
51 n both the discovery and validation cohorts, KS was associated with HLA-A*11:01 (adjusted OR for the
52 nce (Kleaf) and stem hydraulic conductivity (KS).
53 -out coefficients (or Setschenow constants) (KS [M(-1)]) for 38 diverse neutral compounds in ammonium
54 nowledge about Setschenow salting constants, KS, the exponential dependence of Henry's Law coefficien
55  potentially be used in treatment to control KS/PEL.
56                  Moreover, knocking out CPS, KS or CYP112 led to mutant Xoc that exhibited reduced vi
57              During R-Dox therapy, cutaneous KS developed in 1 patient, whereas 5 of 6 patients with
58 r regimens was not associated with decreased KS incidence.
59 iofacial, intellectual, and cardiac defects, KS is also characterized by humoral immune deficiency an
60 We describe a case of probable donor-derived KS in the recipient of a liver-kidney transplant.
61 uthern Africa, Europe and Asia; 26 developed KS after starting cART.
62 idence rates and risk factors for developing KS in different periods after starting cART in patients
63 idence rates and risk factors for developing KS up to 90 and 180 days and 1, 2, 5, and 8 years after
64 ther regions, have a high risk of developing KS after cART initiation.
65 not associated with the hazard of developing KS in the first year after cART initiation, but was over
66 cell counts increased the risk of developing KS throughout all observation periods after cART initiat
67  than those from GGAs or even from the exact KS potential.
68  stable disease, and seven (23.3%) exhibited KS progression.
69 erm generally overpredicted the experimental KS, predicted and experimental values were correlated.
70  We screened STAT4 in additional 18 familial KS cases and the variant site from 56 sporadic KS cases
71 L occurred at higher CD4 counts (P < .05 for KS and NHL) and with undetectable HIV RNA (P < .05 for K
72 ) and with undetectable HIV RNA (P < .05 for KS and NHL).
73 rug has potential as a therapeutic agent for KS.
74 ys provides novel therapeutic approaches for KS tumors.
75 ion, providing novel therapeutic avenues for KS tumors.IMPORTANCE KSHV is the etiologic agent of Kapo
76 ng cART, both incidence and risk factors for KS change with time since starting cART.
77 ests a potential of using YAP inhibitors for KS intervention.
78 The prediction error is generally larger for KS(NaCl) than for KS((NH4)2SO4).
79          Since current treatment methods for KS and PEL are fraught with unwanted side effects and lo
80 othelial cells (LTC) as a cellular model for KS, we demonstrated that KSHV infection induces Nrf2 con
81 al of lipoxin using in vitro cell models for KS and PEL.
82 ld provide potential therapeutic targets for KS.
83 or is generally larger for KS(NaCl) than for KS((NH4)2SO4).
84 Here we show that keratinocytes derived from KS patients are unable to undergo electrotaxis, and this
85 mine whether consuming Lactobacillus gasseri KS-13, Bifidobacterium bifidum G9-1, and B. longum MM-2
86 sitive responses to Stona IB Gel(R), gelatin KS and gelatin RP600, of which the latter two were inclu
87     In this study, we use ketosynthase gene (KS) PCR amplicon sequences (sequence tags) to explore th
88  a simple proof of a theorem: In generalized KS theory (GKS), the band gap of an extended system equa
89 ) theory is shown to be valid in generalized KS theory.
90 ran Africa where approximately 84% of global KS cases occur.
91 V LSSE and the sudden increases in H K and H KS at 175 K are associated with the spin reorientation
92 e perpendicular magnetic anisotropy field (H KS) in the same Pt/YIG system.
93  V LSSE peak at 75 K is attributed to the H KS and M S (saturation magnetization) whose peaks also o
94 es mL (median 72, range <50-74 375); all had KS and 2 also had PEL.
95  act as control valves for species with high KS , or a low safety margin.
96 tro, KS-like mouse tumors and clinical human KS specimens.
97 clear serine-40-phosphorylated Nrf2 in human KS lesions compared to that in healthy tissues.
98 Pomalidomide is well tolerated and active in KS regardless of HIV status.
99 evelopment of organs and tissues affected in KS patients.
100    Despite important ART-related declines in KS incidence, men and women in South Africa and men who
101  and rescued the wound-healing deficiency in KS-TG mice.
102 dlin-1 also failed to rescue electrotaxis in KS cells, indicating that both integrin and lipid bindin
103 the dermal endothelium and hair follicles in KS-TG mice.
104 ceptor/formyl peptidyl receptor (ALX/FPR) in KS patient tissue sections and in vitro KS and PEL cell
105 -like lesions in mice (Rac1), an increase in KS-associated phenotypes (tube formation in endothelial
106 n of antioxidant genes and genes involved in KS pathogenesis such as the NAD(P)H quinone oxidase 1 (N
107 s and mechanisms of action of KSHV miRNAs in KS development.
108  and reduction of SHP1 were also observed in KS patient tissue.
109 d find that glyoxal consistently "salts-in" (KS of -0.16, -0.06, -0.065, -0.1 molality(-1), respectiv
110 clinical cohorts in Europe with 916 incident KS cases.
111 en who have sex with men remain at increased KS risk, likely due to high human herpesvirus 8 coinfect
112 cally active agents, possess a ketosynthase (KS) domain within each module to catalyze chain elongati
113 cyl carrier protein (ACP), and ketosynthase (KS) domains.
114 from a newly developed coupled ketosynthase (KS)-ketoreductase (KR) assay that established that the d
115 denylation (AD) and polyketide ketosynthase (KS) domain fragments amplified from these microbiomes pr
116 lly, we determined that dysfunction of known KS genes and the genes identified in this study results
117                                        Lower KS incidence was observed with longer BPI use, after acc
118     Months on BPIs was associated with lower KS incidence (P = .02).
119                                     The main KS tumor cell is the spindle cell, a cell of endothelial
120                             We have measured KS of glyoxal and methylglyoxal for the atmospherically
121   AIOMFAC tends to underpredict the measured KS((NH4)2SO4) but always overpredicts KS(NaCl).
122 derlying pathogenic mechanism for this novel KS-associated variant.
123  A close correspondence between the observed KS selectivity and that predicted by phylogenetic analys
124 s evidence that KSHV, the etiologic agent of KS, induces aberrant angiogenesis.
125              Supplementation with a blend of KS oil is associated with decreased insulin sensitivity.
126 therwise healthy, received 5 1-g capsules of KS oil or a control (canola oil) for 8 wk and crossed ov
127                                Most cases of KS show a marked reduction or complete absence of the ki
128  of polymicrogyria are not characteristic of KS, and we found only a few previous reports of this ass
129     Kaposi sarcoma (KS) is a complication of KS-associated herpesvirus (KSHV) infection.
130         To date, the precise contribution of KS selectivity in controlling product fidelity has been
131       AIOMFAC also predicted a dependence of KS on the salt concentrations, which is not observed in
132 betic patients contributes to development of KS by promoting KSHV lytic replication and infection.
133 ncogenic activity of KSHV and development of KS, and also suggests a potential of using YAP inhibitor
134 have an important role in the development of KS.
135  showed a mutation in COL18A1, diagnostic of KS.
136  roles of KMT2D and KDM6A in the etiology of KS by using a vertebrate model organism to provide direc
137  harbored within a unique N-terminal exon of KS-WNK1.
138 d testes growth, a characteristic feature of KS.
139 t of structures represents a larger group of KS domains from both canonical and AT-less type I PKSs t
140 s the fundamental gap, a major limitation of KS density-functional theory.
141  KMT2D have been identified in a majority of KS patients, a few patients have mutations in KDM6A.
142 n promoting the aggressive manifestations of KS in AIDS patients; however, the pathogenesis underlyin
143 n promoting the aggressive manifestations of KS, the pathogenesis underlying AIDS-KS remains largely
144 dings provide insights into the mechanism of KS selectivity in this important group of PKSs, can serv
145  cycle) is necessary for the pathogenesis of KS.
146                    The clinical phenotype of KS includes moderate to severe intellectual disability w
147 itical for the initiation and progression of KS.
148 ergic antagonist, decreased proliferation of KS-associated herpesvirus (KSHV)-infected cells.
149                  An increasing proportion of KS and NHL occurred at higher CD4 counts (P < .05 for KS
150 9%; 54 patients have died, 15 as a result of KS.
151  new insight into the potential treatment of KS and PEL using nature's own anti-inflammatory molecule
152 s and long-term benefits of PI-based cART on KS in other cohorts and prospective studies.
153 -control design preclude firm conclusions on KS risk or pathogenesis.
154 owever, effects of cART type and duration on KS remain difficult to interpret secondary to KS-associa
155 KIR influences the risk of KSHV infection or KS.
156 e oral microenvironment plays a role in oral KS tumor development.
157 spectively) while methylglyoxal "salts-out" (KS of +0.16, +0.075, +0.02, +0.06 molality(-1)).
158 asured KS((NH4)2SO4) but always overpredicts KS(NaCl).
159 ed technique (Analyze Direct, Overland Park, KS).
160 ed controlled viremia with either persistent KS despite 3 months of antiretroviral therapy (ART) or p
161 ystal structures of seven AT-less type I PKS KS domains that represent various sequence clusters, rev
162  the structural consequences of a type I PKS KS evolving into an AT-less type I PKS KS.
163 ural diversity within the AT-less type I PKS KS family, and most important, provide a unique opportun
164           Structures of canonical type I PKS KS-AT didomains reveal structured linkers that connect t
165 I PKS KS evolving into an AT-less type I PKS KS.
166 eir substrates, whereas canonical type I PKS KSs are monophyletic.
167                           AT-less type I PKS KSs have remnants of these linkers, which have been hypo
168                           AT-less type I PKS KSs possess substrate specificity and fall into phylogen
169 the current version of COSMOtherm to predict KS.
170 advanced (T1) disease, and 19 (86%) previous KS therapy excluding ART.
171  antiretroviral therapy (ART) or progressive KS despite 2 months of ART.
172 the infected host gene regulation to promote KS pathogenesis.
173 RT initiation in these children might reduce KS risk.
174 nhibitors (BPIs) was associated with reduced KS incidence in the third year of cART (incidence rate r
175 ell counts are essential to further reducing KS incidence worldwide, but additional measures might be
176 er, the pathogenesis underlying AIDS-related KS (AIDS-KS) remains unknown.
177 opsy specimens compared with non-HIV-related KS and NST.
178 lated KS cases compared with non-HIV-related KS and NST.
179 32gamma isoforms was observed in HIV-related KS biopsy specimens compared with non-HIV-related KS and
180 oform, followed by IL-32beta, in HIV-related KS cases compared with non-HIV-related KS and NST.
181 unctional interaction between the respective KS-associated genes and their products in zebrafish mode
182 o dietary potassium loading and restriction, KS-WNK1 knockout mice were deficient in these structures
183 ementation with a blend of krill and salmon (KS) oil [which is rich in eicosapentaenoic acid (EPA) an
184 8) is the causative agent of Kaposi sarcoma (KS) and multicentric Castleman disease (MCD), a life-thr
185                The burden of Kaposi sarcoma (KS) in human immunodeficiency virus (HIV)-infected child
186                              Kaposi sarcoma (KS) incidence has decreased since combination antiretrov
187                              Kaposi sarcoma (KS) is a complication of KS-associated herpesvirus (KSHV
188                              Kaposi sarcoma (KS) remains a frequent cancer in human immunodeficiency
189                  We compared Kaposi sarcoma (KS) risk in adults who started antiretroviral therapy (A
190                              Kaposi sarcoma (KS) risk is affected by perturbed immunity.
191 rit behind the human disease Kaposi sarcoma (KS), an AIDS-defining malignancy.
192 V-related, 7 non-HIV-related Kaposi sarcoma (KS), and 7 normal skin tissues (NSTs) of Dutch origin we
193 V) is the causative agent of Kaposi sarcoma (KS), one of the leading cancers in human immunodeficienc
194 virus (KSHV) is the cause of Kaposi sarcoma (KS), primary effusion lymphoma (PEL), and a form of Cast
195 ) is the causative agent for Kaposi sarcoma (KS), primary effusion lymphoma (PEL), and a subset of mu
196 rstanding of the burden of Kaposi's sarcoma (KS) and non-Hodgkin lymphoma (NHL) relative to antiretro
197                            Kaposi's sarcoma (KS) and primary effusion lymphoma (PEL) are two well-kno
198 ed malignancies, including Kaposi's sarcoma (KS) and primary effusion lymphoma (PEL).
199 an malignancies, including Kaposi's sarcoma (KS) and primary effusion lymphoma (PEL).
200 ed malignancies, including Kaposi's sarcoma (KS) and primary effusion lymphoma (PEL).
201                            Kaposi's sarcoma (KS) as the most common AIDS-associated malignancy is eti
202                            Kaposi's sarcoma (KS) is a disease of multifocal vascular proliferation th
203                    Purpose Kaposi's sarcoma (KS) is a multicentric tumor caused by Kaposi's sarcoma-a
204                            Kaposi's sarcoma (KS) is an AIDS-defining cancer with aberrant neovascular
205                            Kaposi's sarcoma (KS) is common in Africa, but economic constraints hinder
206         High prevalence of Kaposi's sarcoma (KS) is seen in diabetic patients.
207  is the etiologic agent of Kaposi's sarcoma (KS), a vascular tumor frequently found in immunodeficien
208 ologically associated with Kaposi's sarcoma (KS), primary effusion lymphoma (PEL), and multicentric C
209 rus (KSHV) is the cause of Kaposi's sarcoma (KS), which is the most common AIDS-associated malignancy
210                            Kaposi's sarcoma (KS)-associated herpesvirus (KSHV) infection is linked to
211                            Kaposi's sarcoma (KS)-associated herpesvirus (KSHV) is a human gammaherpes
212  the etiological agent for Kaposi's sarcoma (KS).
213 rs for development of oral Kaposi's sarcoma (KS).
214 genic virus that can cause Kaposi's sarcoma (KS).
215  is the etiologic agent of Kaposi's sarcoma (KS).
216 sed individuals, including Kaposi's sarcoma (KS).
217 ffusion lymphoma (PEL) and Kaposi's sarcoma (KS).
218 man herpesvirus 8 (HHV-8) (Kaposi's sarcoma [KS]-associated herpesvirus) and have an important role i
219 was proposed to use the kinetic-segregation (KS) mechanism.
220 cture of the exact multiplicative Kohn-Sham (KS) potential substantially underestimates the fundament
221 pression for the work function in Kohn-Sham (KS) theory is shown to be valid in generalized KS theory
222                                          Six KS domains from trans-acyltransferase (trans-AT) PKSs we
223 gistic regression and by Kolmogorov-Smirnov (KS) statistics.
224  between countries using Kolmogorov-Smirnov (KS) tests, Degree Distribution Quantification and Compar
225                           Potassium sorbate (KS) was chosen as the carrier and two different concentr
226  cases and the variant site from 56 sporadic KS cases but detected no pathogenic mutations.
227 s within the Upper Neosho River subdrainage, KS, from June-August 2013 yielded three generalizable ec
228 rmatan sulfate (CS/DS), and keratan sulfate (KS)-mainly novel glycosylation strategies, elongation se
229 dulatory agent, in patients with symptomatic KS.
230                             Kabuki syndrome (KS) is a complex multisystem developmental disorder asso
231                             Kabuki syndrome (KS) is a rare multiple congenital anomaly syndrome chara
232        The genetic disorder Kabuki syndrome (KS) is characterized by developmental delay and congenit
233 EMA3E) in 2 brothers with Kallmann syndrome (KS), which causes inherited GnRH deficiency.
234                            Kindler syndrome (KS) is an autosomal recessive blistering skin disease re
235                          Kleefstra syndrome (KS) (Mendelian Inheritance in Man (MIM) no.
236 -chromosome (45X), and Klinefelter syndrome (KS), where males have an additional X-chromosome (47XXY)
237                           Knobloch Syndrome (KS) is a rare congenital syndrome characterized by occip
238       Overall 5-year survival was 92% for T0 KS and 83% to T1 KS (P = .0024).
239                             Patients with T0 KS had higher CD4 cell counts (P < .001); 90% of patient
240 l counts (P < .001); 90% of patients with T0 KS who were not receiving cART and 84% of those with T1
241               Patients with early-stage (T0) KS are treated with cART alone; patients with advanced-s
242 ear survival was 92% for T0 KS and 83% to T1 KS (P = .0024).
243  not receiving cART and 84% of those with T1 KS were treated in accordance with the stage-stratified
244 ART alone; patients with advanced-stage (T1) KS receive cART plus liposomal anthracycline chemotherap
245                                 We show that KS values for different salts are additive and present a
246                                          The KS incidence rates were 0/100 000 PYs in children of non
247                                          The KS model postulates that, when small receptors engage th
248                                          The KS test is sensitive to variation in network scale, and
249                                          The KS was successfully treated by switching immunosuppressi
250 0% lower (adjusted OR, 0.6; P = .01) but the KS risk 80% higher with HLA-C group 1 homozygosity (adju
251 the combined cohorts, 0.6; P = .01), but the KS risk was 2-fold higher (adjusted OR, 2.1; P = .002).
252  distributions differed significantly by the KS test.
253 In contrast, recombinant SEMA3E carrying the KS-associated mutation did not protect GnRH neurons from
254              Because IL-1 is abundant in the KS microenvironment and inhibits KSHV replication, this
255 hose whose counts were <50 cells/microL, the KS risk was halved in South Africa (aHR, 0.53; 95% CI, .
256                             Acylation of the KS active site Cys residue is followed by transfer to ma
257 o detailed molecular characterization of the KS-associated immune phenotype has been reported.
258 2 production by T cells and suggest that the KS mechanism contributes to CD28 signaling.
259 Taken together, our studies suggest that the KS pathophysiology overlaps with the RASopathies and pro
260 er the Matsuda index) was 14% lower with the KS oil than with the control oil (P = 0.049).
261                                   Over time, KS and NHL occurred at higher CD4 counts and lower HIV R
262 itivity to electric fields and contribute to KS disease pathology.
263 NAs suppress host proteins and contribute to KS-associated pathogenesis.
264 logical condition of diabetes contributes to KS development.
265  gene expression, ultimately contributing to KS development.
266 d disrupted histone mark binding can lead to KS.
267 nhance KSHV dissemination and progression to KS if infection occurs.
268 o missense mutations in EHMT1 giving rise to KS have been described.
269 S remain difficult to interpret secondary to KS-associated immune reconstitution inflammatory syndrom
270 e and with that the risk for post-transplant KS.
271 on is one of the strategies adopted to treat KS and PEL, a primary motivation for exploring and evalu
272 dels offers a novel possibility for treating KS and PEL with lipoxins.
273 ) in KS patient tissue sections and in vitro KS and PEL cell models offers a novel possibility for tr
274 tors involved in this process using in vitro KS and PEL cells as models.
275 e activated in KSHV-infected cells in vitro, KS-like mouse tumors and clinical human KS specimens.
276  sub-Saharan Africa, a geographic area where KS is highly endemic.
277  using isolates from Western countries-where KS is not endemic.
278 n of the KSHV lytic cycle is associated with KS pathogenesis.
279 e strongly and significantly associated with KS, after adjustment for age and smoking status.
280  KSHV, the etiological agent associated with KS.
281 th complex medical histories consistent with KS in whom next generation sequencing identified the sam
282 shoots, Kleaf was negatively correlated with KS , supporting the HSH.
283 zed 40 individuals clinically diagnosed with KS for mutations in KMT2D and KDM6A.
284               Although several families with KS have been described previously, our case is noteworth
285 issues that are affected in individuals with KS, including craniofacial structures, heart and brain.
286 r proliferation that requires infection with KS herpes virus (KSHV/HHV-8).
287 assess the association of these markers with KS.
288 niparental isodisomy (UPD) in a patient with KS and a de novo, dominant mutation in RAP1B in a second
289 nd we find evidence of only one patient with KS who had an RD identified at an earlier age.
290 nction in a cohort (n = 13) of patients with KS (age, 4 months to 27 years).
291 V-8 MCD and compared them with patients with KS (n = 24) and healthy donors (n = 29).
292              We identified 466 patients with KS and 258 with NHL.
293                            All patients with KS should undergo serial clinical immune evaluations.
294 umoral immune defects found in patients with KS with lysine methyltransferase 2D (KMT2D) mutations.
295                             In patients with KS, autosomal dominant KMT2D mutations are associated wi
296     Chemical probes capable of reacting with KS (ketosynthase)-bound biosynthetic intermediates were
297 RESENTATIONS: We report on two siblings with KS.
298     Here, we show that kidney-specific WNK1 (KS-WNK1), a truncated kinase-defective WNK1 isoform that
299                             In recent years, KS was more frequently diagnosed after ART initiation (5
300 we generated and analyzed 16 unique Zambian, KS-derived, KSHV genomes.

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